A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis

Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Giuseppina Augimeri [verfasserIn] Maria E. Gonzalez [verfasserIn] Alessandro Paolì [verfasserIn] Ahmad Eido [verfasserIn] Yehyun Choi [verfasserIn] Boris Burman [verfasserIn] Sabra Djomehri [verfasserIn] Santhosh Kumar Karthikeyan [verfasserIn] Sooryanarayana Varambally [verfasserIn] Johanna M. Buschhaus [verfasserIn] Yu-Chih Chen [verfasserIn] Loredana Mauro [verfasserIn] Daniela Bonofiglio [verfasserIn] Alexey I. Nesvizhskii [verfasserIn] Gary D. Luker [verfasserIn] Sebastiano Andò [verfasserIn] Euisik Yoon [verfasserIn] Celina G. Kleer [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Cell biology Oncology

Übergeordnetes Werk:	In: JCI Insight - American Society for Clinical investigation, 2020, 8(2023), 18
Übergeordnetes Werk:	volume:8 ; year:2023 ; number:18

Links:	Link aufrufen Link aufrufen Journal toc

Katalog-ID:	DOAJ091026512

Internformat


LEADER	01000caa a22002652 4500
001	DOAJ091026512
003	DE-627
005	20240413222559.0
007	cr uuu---uuuuu
008	240412s2023 xx \|\|\|\|\|o 00\| \|\|eng c
035			\|a (DE-627)DOAJ091026512
035			\|a (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
100	0		\|a Giuseppina Augimeri \|e verfasserin \|4 aut
245	1	2	\|a A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
264		1	\|c 2023
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.
650		4	\|a Cell biology
650		4	\|a Oncology
653		0	\|a Medicine
653		0	\|a R
700	0		\|a Maria E. Gonzalez \|e verfasserin \|4 aut
700	0		\|a Alessandro Paolì \|e verfasserin \|4 aut
700	0		\|a Ahmad Eido \|e verfasserin \|4 aut
700	0		\|a Yehyun Choi \|e verfasserin \|4 aut
700	0		\|a Boris Burman \|e verfasserin \|4 aut
700	0		\|a Sabra Djomehri \|e verfasserin \|4 aut
700	0		\|a Santhosh Kumar Karthikeyan \|e verfasserin \|4 aut
700	0		\|a Sooryanarayana Varambally \|e verfasserin \|4 aut
700	0		\|a Johanna M. Buschhaus \|e verfasserin \|4 aut
700	0		\|a Yu-Chih Chen \|e verfasserin \|4 aut
700	0		\|a Loredana Mauro \|e verfasserin \|4 aut
700	0		\|a Daniela Bonofiglio \|e verfasserin \|4 aut
700	0		\|a Alexey I. Nesvizhskii \|e verfasserin \|4 aut
700	0		\|a Gary D. Luker \|e verfasserin \|4 aut
700	0		\|a Sebastiano Andò \|e verfasserin \|4 aut
700	0		\|a Euisik Yoon \|e verfasserin \|4 aut
700	0		\|a Celina G. Kleer \|e verfasserin \|4 aut
773	0	8	\|i In \|t JCI Insight \|d American Society for Clinical investigation, 2020 \|g 8(2023), 18 \|w (DE-627)872610594 \|w (DE-600)2874757-4 \|x 23793708 \|7 nnns
773	1	8	\|g volume:8 \|g year:2023 \|g number:18
856	4	0	\|u https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be \|z kostenfrei
856	4	0	\|u https://doi.org/10.1172/jci.insight.164216 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/2379-3708 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_60
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 8 \|j 2023 \|e 18

Indexfelder

author_variant	g a ga m e g meg a p ap a e ae y c yc b b bb s d sd s k k skk s v sv j m b jmb y c c ycc l m lm d b db a i n ain g d l gdl s a sa e y ey c g k cgk
matchkey_str	article:23793708:2023----::hbibescnemsnhmltmelouainnacshmr
hierarchy_sort_str	2023
publishDate	2023
allfields	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be DE-627 ger DE-627 rakwb eng Giuseppina Augimeri verfasserin aut A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance. Cell biology Oncology Medicine R Maria E. Gonzalez verfasserin aut Alessandro Paolì verfasserin aut Ahmad Eido verfasserin aut Yehyun Choi verfasserin aut Boris Burman verfasserin aut Sabra Djomehri verfasserin aut Santhosh Kumar Karthikeyan verfasserin aut Sooryanarayana Varambally verfasserin aut Johanna M. Buschhaus verfasserin aut Yu-Chih Chen verfasserin aut Loredana Mauro verfasserin aut Daniela Bonofiglio verfasserin aut Alexey I. Nesvizhskii verfasserin aut Gary D. Luker verfasserin aut Sebastiano Andò verfasserin aut Euisik Yoon verfasserin aut Celina G. Kleer verfasserin aut In JCI Insight American Society for Clinical investigation, 2020 8(2023), 18 (DE-627)872610594 (DE-600)2874757-4 23793708 nnns volume:8 year:2023 number:18 https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be kostenfrei https://doi.org/10.1172/jci.insight.164216 kostenfrei https://doaj.org/toc/2379-3708 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2023 18
spelling	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be DE-627 ger DE-627 rakwb eng Giuseppina Augimeri verfasserin aut A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance. Cell biology Oncology Medicine R Maria E. Gonzalez verfasserin aut Alessandro Paolì verfasserin aut Ahmad Eido verfasserin aut Yehyun Choi verfasserin aut Boris Burman verfasserin aut Sabra Djomehri verfasserin aut Santhosh Kumar Karthikeyan verfasserin aut Sooryanarayana Varambally verfasserin aut Johanna M. Buschhaus verfasserin aut Yu-Chih Chen verfasserin aut Loredana Mauro verfasserin aut Daniela Bonofiglio verfasserin aut Alexey I. Nesvizhskii verfasserin aut Gary D. Luker verfasserin aut Sebastiano Andò verfasserin aut Euisik Yoon verfasserin aut Celina G. Kleer verfasserin aut In JCI Insight American Society for Clinical investigation, 2020 8(2023), 18 (DE-627)872610594 (DE-600)2874757-4 23793708 nnns volume:8 year:2023 number:18 https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be kostenfrei https://doi.org/10.1172/jci.insight.164216 kostenfrei https://doaj.org/toc/2379-3708 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2023 18
allfields_unstemmed	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be DE-627 ger DE-627 rakwb eng Giuseppina Augimeri verfasserin aut A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance. Cell biology Oncology Medicine R Maria E. Gonzalez verfasserin aut Alessandro Paolì verfasserin aut Ahmad Eido verfasserin aut Yehyun Choi verfasserin aut Boris Burman verfasserin aut Sabra Djomehri verfasserin aut Santhosh Kumar Karthikeyan verfasserin aut Sooryanarayana Varambally verfasserin aut Johanna M. Buschhaus verfasserin aut Yu-Chih Chen verfasserin aut Loredana Mauro verfasserin aut Daniela Bonofiglio verfasserin aut Alexey I. Nesvizhskii verfasserin aut Gary D. Luker verfasserin aut Sebastiano Andò verfasserin aut Euisik Yoon verfasserin aut Celina G. Kleer verfasserin aut In JCI Insight American Society for Clinical investigation, 2020 8(2023), 18 (DE-627)872610594 (DE-600)2874757-4 23793708 nnns volume:8 year:2023 number:18 https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be kostenfrei https://doi.org/10.1172/jci.insight.164216 kostenfrei https://doaj.org/toc/2379-3708 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2023 18
allfieldsGer	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be DE-627 ger DE-627 rakwb eng Giuseppina Augimeri verfasserin aut A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance. Cell biology Oncology Medicine R Maria E. Gonzalez verfasserin aut Alessandro Paolì verfasserin aut Ahmad Eido verfasserin aut Yehyun Choi verfasserin aut Boris Burman verfasserin aut Sabra Djomehri verfasserin aut Santhosh Kumar Karthikeyan verfasserin aut Sooryanarayana Varambally verfasserin aut Johanna M. Buschhaus verfasserin aut Yu-Chih Chen verfasserin aut Loredana Mauro verfasserin aut Daniela Bonofiglio verfasserin aut Alexey I. Nesvizhskii verfasserin aut Gary D. Luker verfasserin aut Sebastiano Andò verfasserin aut Euisik Yoon verfasserin aut Celina G. Kleer verfasserin aut In JCI Insight American Society for Clinical investigation, 2020 8(2023), 18 (DE-627)872610594 (DE-600)2874757-4 23793708 nnns volume:8 year:2023 number:18 https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be kostenfrei https://doi.org/10.1172/jci.insight.164216 kostenfrei https://doaj.org/toc/2379-3708 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2023 18
allfieldsSound	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be DE-627 ger DE-627 rakwb eng Giuseppina Augimeri verfasserin aut A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance. Cell biology Oncology Medicine R Maria E. Gonzalez verfasserin aut Alessandro Paolì verfasserin aut Ahmad Eido verfasserin aut Yehyun Choi verfasserin aut Boris Burman verfasserin aut Sabra Djomehri verfasserin aut Santhosh Kumar Karthikeyan verfasserin aut Sooryanarayana Varambally verfasserin aut Johanna M. Buschhaus verfasserin aut Yu-Chih Chen verfasserin aut Loredana Mauro verfasserin aut Daniela Bonofiglio verfasserin aut Alexey I. Nesvizhskii verfasserin aut Gary D. Luker verfasserin aut Sebastiano Andò verfasserin aut Euisik Yoon verfasserin aut Celina G. Kleer verfasserin aut In JCI Insight American Society for Clinical investigation, 2020 8(2023), 18 (DE-627)872610594 (DE-600)2874757-4 23793708 nnns volume:8 year:2023 number:18 https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be kostenfrei https://doi.org/10.1172/jci.insight.164216 kostenfrei https://doaj.org/toc/2379-3708 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2023 18
language	English
source	In JCI Insight 8(2023), 18 volume:8 year:2023 number:18
sourceStr	In JCI Insight 8(2023), 18 volume:8 year:2023 number:18
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Cell biology Oncology Medicine R
isfreeaccess_bool	true
container_title	JCI Insight
authorswithroles_txt_mv	Giuseppina Augimeri @@aut@@ Maria E. Gonzalez @@aut@@ Alessandro Paolì @@aut@@ Ahmad Eido @@aut@@ Yehyun Choi @@aut@@ Boris Burman @@aut@@ Sabra Djomehri @@aut@@ Santhosh Kumar Karthikeyan @@aut@@ Sooryanarayana Varambally @@aut@@ Johanna M. Buschhaus @@aut@@ Yu-Chih Chen @@aut@@ Loredana Mauro @@aut@@ Daniela Bonofiglio @@aut@@ Alexey I. Nesvizhskii @@aut@@ Gary D. Luker @@aut@@ Sebastiano Andò @@aut@@ Euisik Yoon @@aut@@ Celina G. Kleer @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	872610594
id	DOAJ091026512
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ091026512</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413222559.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240412s2023 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ091026512</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Giuseppina Augimeri</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="2"><subfield code="a">A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cell biology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Oncology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">R</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Maria E. Gonzalez</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Alessandro Paolì</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ahmad Eido</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yehyun Choi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Boris Burman</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sabra Djomehri</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Santhosh Kumar Karthikeyan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sooryanarayana Varambally</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Johanna M. Buschhaus</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yu-Chih Chen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Loredana Mauro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Daniela Bonofiglio</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Alexey I. Nesvizhskii</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Gary D. Luker</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sebastiano Andò</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Euisik Yoon</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Celina G. Kleer</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">JCI Insight</subfield><subfield code="d">American Society for Clinical investigation, 2020</subfield><subfield code="g">8(2023), 18</subfield><subfield code="w">(DE-627)872610594</subfield><subfield code="w">(DE-600)2874757-4</subfield><subfield code="x">23793708</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:8</subfield><subfield code="g">year:2023</subfield><subfield code="g">number:18</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1172/jci.insight.164216</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2379-3708</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">8</subfield><subfield code="j">2023</subfield><subfield code="e">18</subfield></datafield></record></collection>
author	Giuseppina Augimeri
spellingShingle	Giuseppina Augimeri misc Cell biology misc Oncology misc Medicine misc R A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
authorStr	Giuseppina Augimeri
ppnlink_with_tag_str_mv	@@773@@(DE-627)872610594
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut
collection	DOAJ
remote_str	true
illustrated	Not Illustrated
issn	23793708
topic_title	A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis Cell biology Oncology
topic	misc Cell biology misc Oncology misc Medicine misc R
topic_unstemmed	misc Cell biology misc Oncology misc Medicine misc R
topic_browse	misc Cell biology misc Oncology misc Medicine misc R
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	JCI Insight
hierarchy_parent_id	872610594
hierarchy_top_title	JCI Insight
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)872610594 (DE-600)2874757-4
title	A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
ctrlnum	(DE-627)DOAJ091026512 (DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be
title_full	A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
author_sort	Giuseppina Augimeri
journal	JCI Insight
journalStr	JCI Insight
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2023
contenttype_str_mv	txt
author_browse	Giuseppina Augimeri Maria E. Gonzalez Alessandro Paolì Ahmad Eido Yehyun Choi Boris Burman Sabra Djomehri Santhosh Kumar Karthikeyan Sooryanarayana Varambally Johanna M. Buschhaus Yu-Chih Chen Loredana Mauro Daniela Bonofiglio Alexey I. Nesvizhskii Gary D. Luker Sebastiano Andò Euisik Yoon Celina G. Kleer
container_volume	8
format_se	Elektronische Aufsätze
author-letter	Giuseppina Augimeri
author2-role	verfasserin
title_sort	hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
title_auth	A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
abstract	Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.
abstractGer	Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.
abstract_unstemmed	Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	18
title_short	A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis
url	https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be https://doi.org/10.1172/jci.insight.164216 https://doaj.org/toc/2379-3708
remote_bool	true
author2	Maria E. Gonzalez Alessandro Paolì Ahmad Eido Yehyun Choi Boris Burman Sabra Djomehri Santhosh Kumar Karthikeyan Sooryanarayana Varambally Johanna M. Buschhaus Yu-Chih Chen Loredana Mauro Daniela Bonofiglio Alexey I. Nesvizhskii Gary D. Luker Sebastiano Andò Euisik Yoon Celina G. Kleer
author2Str	Maria E. Gonzalez Alessandro Paolì Ahmad Eido Yehyun Choi Boris Burman Sabra Djomehri Santhosh Kumar Karthikeyan Sooryanarayana Varambally Johanna M. Buschhaus Yu-Chih Chen Loredana Mauro Daniela Bonofiglio Alexey I. Nesvizhskii Gary D. Luker Sebastiano Andò Euisik Yoon Celina G. Kleer
ppnlink	872610594
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
up_date	2024-07-03T17:59:44.302Z
_version_	1803581741391151104
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ091026512</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413222559.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240412s2023 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ091026512</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ0fdb611aabcf4f8398eea1d60e3165be</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Giuseppina Augimeri</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="2"><subfield code="a">A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with triple-negative breast cancer remain at risk for metastatic disease despite treatment. The acquisition of chemoresistance is a major cause of tumor relapse and death, but the mechanisms are far from understood. We have demonstrated that breast cancer cells (BCCs) can engulf mesenchymal stem/stromal cells (MSCs), leading to enhanced dissemination. Here, we show that clinical samples of primary invasive carcinoma and chemoresistant breast cancer metastasis contain a unique hybrid cancer cell population coexpressing pancytokeratin and the MSC marker fibroblast activation protein-α. We show that hybrid cells form in primary tumors and that they promote breast cancer metastasis and chemoresistance. Using single-cell microfluidics and in vivo models, we found that there are polyploid senescent cells within the hybrid cell population that contribute to metastatic dissemination. Our data reveal that Wnt Family Member 5A (WNT5A) plays a crucial role in supporting the chemoresistance properties of hybrid cells. Furthermore, we identified that WNT5A mediates hybrid cell formation through a phagocytosis-like mechanism that requires BCC-derived IL-6 and MSC-derived C-C Motif Chemokine Ligand 2. These findings reveal hybrid cell formation as a mechanism of chemoresistance and suggest that interrupting this mechanism may be a strategy in overcoming breast cancer drug resistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cell biology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Oncology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">R</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Maria E. Gonzalez</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Alessandro Paolì</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ahmad Eido</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yehyun Choi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Boris Burman</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sabra Djomehri</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Santhosh Kumar Karthikeyan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sooryanarayana Varambally</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Johanna M. Buschhaus</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yu-Chih Chen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Loredana Mauro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Daniela Bonofiglio</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Alexey I. Nesvizhskii</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Gary D. Luker</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sebastiano Andò</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Euisik Yoon</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Celina G. Kleer</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">JCI Insight</subfield><subfield code="d">American Society for Clinical investigation, 2020</subfield><subfield code="g">8(2023), 18</subfield><subfield code="w">(DE-627)872610594</subfield><subfield code="w">(DE-600)2874757-4</subfield><subfield code="x">23793708</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:8</subfield><subfield code="g">year:2023</subfield><subfield code="g">number:18</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/0fdb611aabcf4f8398eea1d60e3165be</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1172/jci.insight.164216</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2379-3708</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">8</subfield><subfield code="j">2023</subfield><subfield code="e">18</subfield></datafield></record></collection>
score	7.4006186

Nicht das Richtige dabei?

Schreiben Sie uns!

A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?