Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer

Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tiss...
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Autor*in:	Lin Shi [verfasserIn] Weiliang Zhu [verfasserIn] Yuanyuan Huang [verfasserIn] Lin Zhuo [verfasserIn] Siyun Wang [verfasserIn] Shaobing Chen [verfasserIn] Bei Zhang [verfasserIn] Bin Ke [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	CAF exosome microRNA‐20a NSCLC PTEN

Übergeordnetes Werk:	In: Clinical and Translational Medicine - Wiley, 2013, 12(2022), 7, Seite n/a-n/a
Übergeordnetes Werk:	volume:12 ; year:2022 ; number:7 ; pages:n/a-n/a

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/ctm2.989

Katalog-ID:	DOAJ040304213

Internformat


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245	1	0	\|a Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
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520			\|a Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC.
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700	0		\|a Bin Ke \|e verfasserin \|4 aut
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allfields	10.1002/ctm2.989 doi (DE-627)DOAJ040304213 (DE-599)DOAJ70c2722a3c0445449c3209544fa24a36 DE-627 ger DE-627 rakwb eng R5-920 Lin Shi verfasserin aut Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC. CAF exosome microRNA‐20a NSCLC PTEN Medicine (General) Weiliang Zhu verfasserin aut Yuanyuan Huang verfasserin aut Lin Zhuo verfasserin aut Siyun Wang verfasserin aut Shaobing Chen verfasserin aut Bei Zhang verfasserin aut Bin Ke verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 7, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:7 pages:n/a-n/a https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 kostenfrei https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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 12 2022 7 n/a-n/a
spelling	10.1002/ctm2.989 doi (DE-627)DOAJ040304213 (DE-599)DOAJ70c2722a3c0445449c3209544fa24a36 DE-627 ger DE-627 rakwb eng R5-920 Lin Shi verfasserin aut Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC. CAF exosome microRNA‐20a NSCLC PTEN Medicine (General) Weiliang Zhu verfasserin aut Yuanyuan Huang verfasserin aut Lin Zhuo verfasserin aut Siyun Wang verfasserin aut Shaobing Chen verfasserin aut Bei Zhang verfasserin aut Bin Ke verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 7, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:7 pages:n/a-n/a https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 kostenfrei https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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 12 2022 7 n/a-n/a
allfields_unstemmed	10.1002/ctm2.989 doi (DE-627)DOAJ040304213 (DE-599)DOAJ70c2722a3c0445449c3209544fa24a36 DE-627 ger DE-627 rakwb eng R5-920 Lin Shi verfasserin aut Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC. CAF exosome microRNA‐20a NSCLC PTEN Medicine (General) Weiliang Zhu verfasserin aut Yuanyuan Huang verfasserin aut Lin Zhuo verfasserin aut Siyun Wang verfasserin aut Shaobing Chen verfasserin aut Bei Zhang verfasserin aut Bin Ke verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 7, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:7 pages:n/a-n/a https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 kostenfrei https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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 12 2022 7 n/a-n/a
allfieldsGer	10.1002/ctm2.989 doi (DE-627)DOAJ040304213 (DE-599)DOAJ70c2722a3c0445449c3209544fa24a36 DE-627 ger DE-627 rakwb eng R5-920 Lin Shi verfasserin aut Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC. CAF exosome microRNA‐20a NSCLC PTEN Medicine (General) Weiliang Zhu verfasserin aut Yuanyuan Huang verfasserin aut Lin Zhuo verfasserin aut Siyun Wang verfasserin aut Shaobing Chen verfasserin aut Bei Zhang verfasserin aut Bin Ke verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 7, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:7 pages:n/a-n/a https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 kostenfrei https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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 12 2022 7 n/a-n/a
allfieldsSound	10.1002/ctm2.989 doi (DE-627)DOAJ040304213 (DE-599)DOAJ70c2722a3c0445449c3209544fa24a36 DE-627 ger DE-627 rakwb eng R5-920 Lin Shi verfasserin aut Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC. CAF exosome microRNA‐20a NSCLC PTEN Medicine (General) Weiliang Zhu verfasserin aut Yuanyuan Huang verfasserin aut Lin Zhuo verfasserin aut Siyun Wang verfasserin aut Shaobing Chen verfasserin aut Bei Zhang verfasserin aut Bin Ke verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 7, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:7 pages:n/a-n/a https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 kostenfrei https://doi.org/10.1002/ctm2.989 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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 12 2022 7 n/a-n/a
language	English
source	In Clinical and Translational Medicine 12(2022), 7, Seite n/a-n/a volume:12 year:2022 number:7 pages:n/a-n/a
sourceStr	In Clinical and Translational Medicine 12(2022), 7, Seite n/a-n/a volume:12 year:2022 number:7 pages:n/a-n/a
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	CAF exosome microRNA‐20a NSCLC PTEN Medicine (General)
isfreeaccess_bool	true
container_title	Clinical and Translational Medicine
authorswithroles_txt_mv	Lin Shi @@aut@@ Weiliang Zhu @@aut@@ Yuanyuan Huang @@aut@@ Lin Zhuo @@aut@@ Siyun Wang @@aut@@ Shaobing Chen @@aut@@ Bei Zhang @@aut@@ Bin Ke @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	733752837
id	DOAJ040304213
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">DOAJ040304213</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503063718.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ctm2.989</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ040304213</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ70c2722a3c0445449c3209544fa24a36</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="050" ind1=" " ind2="0"><subfield code="a">R5-920</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Lin Shi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</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 Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CAF</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">exosome</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">microRNA‐20a</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">NSCLC</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">PTEN</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Weiliang Zhu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield 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callnumber-first	R - Medicine
author	Lin Shi
spellingShingle	Lin Shi misc R5-920 misc CAF misc exosome misc microRNA‐20a misc NSCLC misc PTEN misc Medicine (General) Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
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topic_title	R5-920 Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer CAF exosome microRNA‐20a NSCLC PTEN
topic	misc R5-920 misc CAF misc exosome misc microRNA‐20a misc NSCLC misc PTEN misc Medicine (General)
topic_unstemmed	misc R5-920 misc CAF misc exosome misc microRNA‐20a misc NSCLC misc PTEN misc Medicine (General)
topic_browse	misc R5-920 misc CAF misc exosome misc microRNA‐20a misc NSCLC misc PTEN misc Medicine (General)
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title	Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
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title_full	Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
author_sort	Lin Shi
journal	Clinical and Translational Medicine
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author_browse	Lin Shi Weiliang Zhu Yuanyuan Huang Lin Zhuo Siyun Wang Shaobing Chen Bei Zhang Bin Ke
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title_sort	cancer‐associated fibroblast‐derived exosomal microrna‐20a suppresses the pten/pi3k‐akt pathway to promote the progression and chemoresistance of non‐small cell lung cancer
callnumber	R5-920
title_auth	Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
abstract	Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC.
abstractGer	Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC.
abstract_unstemmed	Abstract Background Cancer‐associated fibroblasts (CAFs) contributes to overall tumor progression. In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. Conclusion The achieved outcomes explain that CAFs can release miR‐20a‐containing exosomes capable of promoting NSCLC progression and chemoresistance, highlighting this pathway as a possible therapeutic target in NSCLC.
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title_short	Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer
url	https://doi.org/10.1002/ctm2.989 https://doaj.org/article/70c2722a3c0445449c3209544fa24a36 https://doaj.org/toc/2001-1326
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up_date	2024-07-03T14:06:07.529Z
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In the current survey, we explored the ability of microRNA‐20a (miR‐20a) within these CAF‐derived exosomes to influence non‐small‐cell lung cancer (NSCLC) progression. Materials and methods Normal tissue‐associated fibroblasts (NAFs) and CAFs were collected from samples of NSCLC patient tumors and paracancerous lung tissues. Exosomes derived from these cells were then characterized via Western blotting, nanoparticle tracking analyses, and transmission electron microscopy. The expression of miR‐20a was assessed via qPCR and fluorescence in situ hybridization (FISH). CCK‐8, EdU uptake, and colony formation assessments were used for evaluating tumor proliferation, while Hoechst staining was performed to monitor the in vitro apoptotic death of tumor cells. A model of xenograft tumor established in nude mice was also used to evaluate in vivo tumor responses. Results CAF‐derived exosomes exhibited miR‐20a upregulation and promoted NSCLC cell proliferation and resistance to cisplatin (DDP). Mechanistically, CAF‐derived exosomes were discovered to transmit miR‐20a to tumor cells wherein it was able to target PTEN to enhance DDP resistance and proliferation. Associated PTEN downregulation following exosome‐derived miR‐20a treatment enhanced PI3K/AKT pathway activation. 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Cancer‐associated fibroblast‐derived exosomal microRNA‐20a suppresses the PTEN/PI3K‐AKT pathway to promote the progression and chemoresistance of non‐small cell lung cancer

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