CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy

Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ...
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Autor*in:	Yuncheng Bei [verfasserIn] Nan Cheng [verfasserIn] Ting Chen [verfasserIn] Yuxin Shu [verfasserIn] Ye Yang [verfasserIn] Nanfei Yang [verfasserIn] Xinyu Zhou [verfasserIn] Baorui Liu [verfasserIn] Jia Wei [verfasserIn] Qin Liu [verfasserIn] Wei Zheng [verfasserIn] Wenlong Zhang [verfasserIn] Huifang Su [verfasserIn] Wei‐Guo Zhu [verfasserIn] Jianguo Ji [verfasserIn] Pingping Shen [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer

Übergeordnetes Werk:	In: Advanced Science - Wiley, 2015, 7(2020), 22, Seite n/a-n/a
Übergeordnetes Werk:	volume:7 ; year:2020 ; number:22 ; pages:n/a-n/a

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/advs.202001417

Katalog-ID:	DOAJ006478883

Internformat


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520			\|a Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy.
650		4	\|a cancer stem cells
650		4	\|a CD44 variants
650		4	\|a CDK5
650		4	\|a immune checkpoint blockade
650		4	\|a PPARγ phosphorylation
650		4	\|a triple‐negative breast cancer
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700	0		\|a Jia Wei \|e verfasserin \|4 aut
700	0		\|a Qin Liu \|e verfasserin \|4 aut
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700	0		\|a Wenlong Zhang \|e verfasserin \|4 aut
700	0		\|a Huifang Su \|e verfasserin \|4 aut
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700	0		\|a Jianguo Ji \|e verfasserin \|4 aut
700	0		\|a Pingping Shen \|e verfasserin \|4 aut
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Indexfelder

author_variant	y b yb n c nc t c tc y s ys y y yy n y ny x z xz b l bl j w jw q l ql w z wz w z wz h s hs w z wz j j jj p s ps
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publishDate	2020
allfields	10.1002/advs.202001417 doi (DE-627)DOAJ006478883 (DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22 DE-627 ger DE-627 rakwb eng Yuncheng Bei verfasserin aut CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy. cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q Nan Cheng verfasserin aut Ting Chen verfasserin aut Yuxin Shu verfasserin aut Ye Yang verfasserin aut Nanfei Yang verfasserin aut Xinyu Zhou verfasserin aut Baorui Liu verfasserin aut Jia Wei verfasserin aut Qin Liu verfasserin aut Wei Zheng verfasserin aut Wenlong Zhang verfasserin aut Huifang Su verfasserin aut Wei‐Guo Zhu verfasserin aut Jianguo Ji verfasserin aut Pingping Shen verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 kostenfrei https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a
spelling	10.1002/advs.202001417 doi (DE-627)DOAJ006478883 (DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22 DE-627 ger DE-627 rakwb eng Yuncheng Bei verfasserin aut CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy. cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q Nan Cheng verfasserin aut Ting Chen verfasserin aut Yuxin Shu verfasserin aut Ye Yang verfasserin aut Nanfei Yang verfasserin aut Xinyu Zhou verfasserin aut Baorui Liu verfasserin aut Jia Wei verfasserin aut Qin Liu verfasserin aut Wei Zheng verfasserin aut Wenlong Zhang verfasserin aut Huifang Su verfasserin aut Wei‐Guo Zhu verfasserin aut Jianguo Ji verfasserin aut Pingping Shen verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 kostenfrei https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a
allfields_unstemmed	10.1002/advs.202001417 doi (DE-627)DOAJ006478883 (DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22 DE-627 ger DE-627 rakwb eng Yuncheng Bei verfasserin aut CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy. cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q Nan Cheng verfasserin aut Ting Chen verfasserin aut Yuxin Shu verfasserin aut Ye Yang verfasserin aut Nanfei Yang verfasserin aut Xinyu Zhou verfasserin aut Baorui Liu verfasserin aut Jia Wei verfasserin aut Qin Liu verfasserin aut Wei Zheng verfasserin aut Wenlong Zhang verfasserin aut Huifang Su verfasserin aut Wei‐Guo Zhu verfasserin aut Jianguo Ji verfasserin aut Pingping Shen verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 kostenfrei https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a
allfieldsGer	10.1002/advs.202001417 doi (DE-627)DOAJ006478883 (DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22 DE-627 ger DE-627 rakwb eng Yuncheng Bei verfasserin aut CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy. cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q Nan Cheng verfasserin aut Ting Chen verfasserin aut Yuxin Shu verfasserin aut Ye Yang verfasserin aut Nanfei Yang verfasserin aut Xinyu Zhou verfasserin aut Baorui Liu verfasserin aut Jia Wei verfasserin aut Qin Liu verfasserin aut Wei Zheng verfasserin aut Wenlong Zhang verfasserin aut Huifang Su verfasserin aut Wei‐Guo Zhu verfasserin aut Jianguo Ji verfasserin aut Pingping Shen verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 kostenfrei https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a
allfieldsSound	10.1002/advs.202001417 doi (DE-627)DOAJ006478883 (DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22 DE-627 ger DE-627 rakwb eng Yuncheng Bei verfasserin aut CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy. cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q Nan Cheng verfasserin aut Ting Chen verfasserin aut Yuxin Shu verfasserin aut Ye Yang verfasserin aut Nanfei Yang verfasserin aut Xinyu Zhou verfasserin aut Baorui Liu verfasserin aut Jia Wei verfasserin aut Qin Liu verfasserin aut Wei Zheng verfasserin aut Wenlong Zhang verfasserin aut Huifang Su verfasserin aut Wei‐Guo Zhu verfasserin aut Jianguo Ji verfasserin aut Pingping Shen verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 kostenfrei https://doi.org/10.1002/advs.202001417 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a
language	English
source	In Advanced Science 7(2020), 22, Seite n/a-n/a volume:7 year:2020 number:22 pages:n/a-n/a
sourceStr	In Advanced Science 7(2020), 22, Seite n/a-n/a volume:7 year:2020 number:22 pages:n/a-n/a
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer Science Q
isfreeaccess_bool	true
container_title	Advanced Science
authorswithroles_txt_mv	Yuncheng Bei @@aut@@ Nan Cheng @@aut@@ Ting Chen @@aut@@ Yuxin Shu @@aut@@ Ye Yang @@aut@@ Nanfei Yang @@aut@@ Xinyu Zhou @@aut@@ Baorui Liu @@aut@@ Jia Wei @@aut@@ Qin Liu @@aut@@ Wei Zheng @@aut@@ Wenlong Zhang @@aut@@ Huifang Su @@aut@@ Wei‐Guo Zhu @@aut@@ Jianguo Ji @@aut@@ Pingping Shen @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	817357777
id	DOAJ006478883
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">DOAJ006478883</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309203905.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/advs.202001417</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ006478883</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ246c50f459d94f8ab89eb2dbed23ab22</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">Yuncheng Bei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</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">Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. 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author	Yuncheng Bei
spellingShingle	Yuncheng Bei misc cancer stem cells misc CD44 variants misc CDK5 misc immune checkpoint blockade misc PPARγ phosphorylation misc triple‐negative breast cancer misc Science misc Q CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy
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topic_title	CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy cancer stem cells CD44 variants CDK5 immune checkpoint blockade PPARγ phosphorylation triple‐negative breast cancer
topic	misc cancer stem cells misc CD44 variants misc CDK5 misc immune checkpoint blockade misc PPARγ phosphorylation misc triple‐negative breast cancer misc Science misc Q
topic_unstemmed	misc cancer stem cells misc CD44 variants misc CDK5 misc immune checkpoint blockade misc PPARγ phosphorylation misc triple‐negative breast cancer misc Science misc Q
topic_browse	misc cancer stem cells misc CD44 variants misc CDK5 misc immune checkpoint blockade misc PPARγ phosphorylation misc triple‐negative breast cancer misc Science misc Q
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title	CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy
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title_full	CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy
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author_browse	Yuncheng Bei Nan Cheng Ting Chen Yuxin Shu Ye Yang Nanfei Yang Xinyu Zhou Baorui Liu Jia Wei Qin Liu Wei Zheng Wenlong Zhang Huifang Su Wei‐Guo Zhu Jianguo Ji Pingping Shen
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title_sort	cdk5 inhibition abrogates tnbc stem‐cell property and enhances anti‐pd‐1 therapy
title_auth	CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy
abstract	Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy.
abstractGer	Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy.
abstract_unstemmed	Abstract Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which the higher frequency of cancer stem cells (CSCs) correlates with the poor clinical outcome. An aberrant activation of CDK5 is found to associate with TNBC progression closely. CDK5 mediates PPARγ phosphorylation at its Ser 273, which induces CD44 isoform switching from CD44s to CD44v, resulting in an increase of stemness of TNBC cells. Blocking CDK5/pho‐PPARγ significantly reduces CD44v+ BCSCs population in tumor tissues, thus abrogating metastatic progression in TNBC mouse model. Strikingly, diminishing stemness transformation reverses immunosuppressive microenvironment and enhances anti‐PD‐1 therapeutic efficacy on TNBC. Mechanistically, CDK5 switches the E3 ubiquitin ligase activity of PPARγ and directly protects ESRP1 from a ubiquitin‐dependent proteolysis. This finding firstly indicates that CDK5 blockade can be a potent strategy to diminish stemness transformation and increase the response to PD‐1 blockade in TNBC therapy.
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title_short	CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy
url	https://doi.org/10.1002/advs.202001417 https://doaj.org/article/246c50f459d94f8ab89eb2dbed23ab22 https://doaj.org/toc/2198-3844
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up_date	2024-07-03T21:10:23.509Z
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CDK5 Inhibition Abrogates TNBC Stem‐Cell Property and Enhances Anti‐PD‐1 Therapy

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