Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation
•PTMA expression is significantly increased in CRC patients.•PTMA enhances LD accumulation in CRC cells.•PTMA-dependent LD production facilitates CRC chemoresistance.•PTMA promotes chemoresistance by regulating SREBP-1-mediated lipogenesis.•PTMA promotes the acetylation and activation of STAT3 to su...
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| Veröffentlicht in: | Mitochondrion 2021-07, Vol.59, p.123-134 |
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| creator | Jin, Long Zhu, Li-Yong Pan, Yu-Liang Fu, Hui-Qun Zhang, Jun |
| description | •PTMA expression is significantly increased in CRC patients.•PTMA enhances LD accumulation in CRC cells.•PTMA-dependent LD production facilitates CRC chemoresistance.•PTMA promotes chemoresistance by regulating SREBP-1-mediated lipogenesis.•PTMA promotes the acetylation and activation of STAT3 to support LD biogenesis and chemoresistance.
Colorectal cancer (CRC) affects millions of people worldwide. Chemoresistance seriously impairs the therapeutic effects. Lipid droplets (LDs) abnormally accumulate in CRC supported chemoresistance. Exploring the mechanism of LD-induced chemoresistance is extremely important for improving prognosis of CRC patients. The expression of PTMA was increased in both CRC tissues and cells, which was positively correlated with LD production. PTMA facilitated chemoresistance to gemcitabine by inducing LD production in CRC cells. PTMA enhanced LD biogenesis and chemoresistance to gemcitabine by promoting SREBP-1-mediated lipogenesis and STAT3 activation in CRC. |
| doi_str_mv | 10.1016/j.mito.2021.04.001 |
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Colorectal cancer (CRC) affects millions of people worldwide. Chemoresistance seriously impairs the therapeutic effects. Lipid droplets (LDs) abnormally accumulate in CRC supported chemoresistance. Exploring the mechanism of LD-induced chemoresistance is extremely important for improving prognosis of CRC patients. The expression of PTMA was increased in both CRC tissues and cells, which was positively correlated with LD production. PTMA facilitated chemoresistance to gemcitabine by inducing LD production in CRC cells. PTMA enhanced LD biogenesis and chemoresistance to gemcitabine by promoting SREBP-1-mediated lipogenesis and STAT3 activation in CRC.</description><identifier>ISSN: 1567-7249</identifier><identifier>EISSN: 1872-8278</identifier><identifier>DOI: 10.1016/j.mito.2021.04.001</identifier><identifier>PMID: 33872798</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Acetylation ; Caco-2 Cells ; Cell Line, Tumor ; Colonic Neoplasms - drug therapy ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colorectal carcinoma chemoresistance ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; HT29 Cells ; Humans ; Lipid droplet ; Lipid Droplets - metabolism ; Lipogenesis ; Prognosis ; Protein Precursors - genetics ; Protein Precursors - metabolism ; Prothymosin α/PTMA ; SREBP-1 ; STAT3 ; STAT3 Transcription Factor - metabolism ; Sterol Regulatory Element Binding Protein 1 - genetics ; Sterol Regulatory Element Binding Protein 1 - metabolism ; Thymosin - analogs & derivatives ; Thymosin - genetics ; Thymosin - metabolism ; Up-Regulation</subject><ispartof>Mitochondrion, 2021-07, Vol.59, p.123-134</ispartof><rights>2021 Elsevier B.V. and Mitochondria Research Society</rights><rights>Copyright © 2021 Elsevier B.V. and Mitochondria Research Society. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-4ad8eebcea8036c1cfe15945e7c5b4e8d8a79d33f9f48f88bca9686653542a3f3</citedby><cites>FETCH-LOGICAL-c356t-4ad8eebcea8036c1cfe15945e7c5b4e8d8a79d33f9f48f88bca9686653542a3f3</cites><orcidid>0000-0002-3440-9299</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.mito.2021.04.001$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33872798$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jin, Long</creatorcontrib><creatorcontrib>Zhu, Li-Yong</creatorcontrib><creatorcontrib>Pan, Yu-Liang</creatorcontrib><creatorcontrib>Fu, Hui-Qun</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><title>Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation</title><title>Mitochondrion</title><addtitle>Mitochondrion</addtitle><description>•PTMA expression is significantly increased in CRC patients.•PTMA enhances LD accumulation in CRC cells.•PTMA-dependent LD production facilitates CRC chemoresistance.•PTMA promotes chemoresistance by regulating SREBP-1-mediated lipogenesis.•PTMA promotes the acetylation and activation of STAT3 to support LD biogenesis and chemoresistance.
Colorectal cancer (CRC) affects millions of people worldwide. Chemoresistance seriously impairs the therapeutic effects. Lipid droplets (LDs) abnormally accumulate in CRC supported chemoresistance. Exploring the mechanism of LD-induced chemoresistance is extremely important for improving prognosis of CRC patients. The expression of PTMA was increased in both CRC tissues and cells, which was positively correlated with LD production. PTMA facilitated chemoresistance to gemcitabine by inducing LD production in CRC cells. PTMA enhanced LD biogenesis and chemoresistance to gemcitabine by promoting SREBP-1-mediated lipogenesis and STAT3 activation in CRC.</description><subject>Acetylation</subject><subject>Caco-2 Cells</subject><subject>Cell Line, Tumor</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal carcinoma chemoresistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HCT116 Cells</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Lipid droplet</subject><subject>Lipid Droplets - metabolism</subject><subject>Lipogenesis</subject><subject>Prognosis</subject><subject>Protein Precursors - genetics</subject><subject>Protein Precursors - metabolism</subject><subject>Prothymosin α/PTMA</subject><subject>SREBP-1</subject><subject>STAT3</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Sterol Regulatory Element Binding Protein 1 - genetics</subject><subject>Sterol Regulatory Element Binding Protein 1 - metabolism</subject><subject>Thymosin - analogs & derivatives</subject><subject>Thymosin - genetics</subject><subject>Thymosin - metabolism</subject><subject>Up-Regulation</subject><issn>1567-7249</issn><issn>1872-8278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM9qFTEUh4MotlZfwIVk6WbG_J1kwI0UWwsFu9B1yE3OdHKZTK5JRuhj9UV8JnO51WVX53D4fj84H0LvKekpocOnfR9DTT0jjPZE9ITQF-icasU6zZR-2XY5qE4xMZ6hN6XsG6AoY6_RGeeNUqM-R_NdTnV-iKmEFf95xIecYqpQsEtLyuCqXbCz2YU1RYvdDLFdSyjVrg5wnXPa7mccVr815B4v4RA89jkdFqjYOrfFbbE1pPUtejXZpcC7p3mBfl59_XH5rbv9fn1z-eW2c1wOtRPWa4CdA6sJHxx1E1A5CgnKyZ0A7bVVo-d8GiehJ613zo6DHgbJpWCWT_wCfTz1tk9-bVCqiaE4WBa7QtqKYbJZ0VII1VB2Ql1OpWSYzCGHaPODocQcDZu9ORo2R8OGCNMEttCHp_5tF8H_j_xT2oDPJwDal78DZFNcgGbLh6NP41N4rv8vCjqRHA</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Jin, Long</creator><creator>Zhu, Li-Yong</creator><creator>Pan, Yu-Liang</creator><creator>Fu, Hui-Qun</creator><creator>Zhang, Jun</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3440-9299</orcidid></search><sort><creationdate>202107</creationdate><title>Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation</title><author>Jin, Long ; Zhu, Li-Yong ; Pan, Yu-Liang ; Fu, Hui-Qun ; Zhang, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-4ad8eebcea8036c1cfe15945e7c5b4e8d8a79d33f9f48f88bca9686653542a3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acetylation</topic><topic>Caco-2 Cells</topic><topic>Cell Line, Tumor</topic><topic>Colonic Neoplasms - drug therapy</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colorectal carcinoma chemoresistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HCT116 Cells</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Lipid droplet</topic><topic>Lipid Droplets - metabolism</topic><topic>Lipogenesis</topic><topic>Prognosis</topic><topic>Protein Precursors - genetics</topic><topic>Protein Precursors - metabolism</topic><topic>Prothymosin α/PTMA</topic><topic>SREBP-1</topic><topic>STAT3</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Sterol Regulatory Element Binding Protein 1 - genetics</topic><topic>Sterol Regulatory Element Binding Protein 1 - metabolism</topic><topic>Thymosin - analogs & derivatives</topic><topic>Thymosin - genetics</topic><topic>Thymosin - metabolism</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Long</creatorcontrib><creatorcontrib>Zhu, Li-Yong</creatorcontrib><creatorcontrib>Pan, Yu-Liang</creatorcontrib><creatorcontrib>Fu, Hui-Qun</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Mitochondrion</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Long</au><au>Zhu, Li-Yong</au><au>Pan, Yu-Liang</au><au>Fu, Hui-Qun</au><au>Zhang, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation</atitle><jtitle>Mitochondrion</jtitle><addtitle>Mitochondrion</addtitle><date>2021-07</date><risdate>2021</risdate><volume>59</volume><spage>123</spage><epage>134</epage><pages>123-134</pages><issn>1567-7249</issn><eissn>1872-8278</eissn><abstract>•PTMA expression is significantly increased in CRC patients.•PTMA enhances LD accumulation in CRC cells.•PTMA-dependent LD production facilitates CRC chemoresistance.•PTMA promotes chemoresistance by regulating SREBP-1-mediated lipogenesis.•PTMA promotes the acetylation and activation of STAT3 to support LD biogenesis and chemoresistance.
Colorectal cancer (CRC) affects millions of people worldwide. Chemoresistance seriously impairs the therapeutic effects. Lipid droplets (LDs) abnormally accumulate in CRC supported chemoresistance. Exploring the mechanism of LD-induced chemoresistance is extremely important for improving prognosis of CRC patients. The expression of PTMA was increased in both CRC tissues and cells, which was positively correlated with LD production. PTMA facilitated chemoresistance to gemcitabine by inducing LD production in CRC cells. PTMA enhanced LD biogenesis and chemoresistance to gemcitabine by promoting SREBP-1-mediated lipogenesis and STAT3 activation in CRC.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>33872798</pmid><doi>10.1016/j.mito.2021.04.001</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-3440-9299</orcidid></addata></record> |
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| subjects | Acetylation Caco-2 Cells Cell Line, Tumor Colonic Neoplasms - drug therapy Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colorectal carcinoma chemoresistance Drug Resistance, Neoplasm Gene Expression Regulation, Neoplastic HCT116 Cells HT29 Cells Humans Lipid droplet Lipid Droplets - metabolism Lipogenesis Prognosis Protein Precursors - genetics Protein Precursors - metabolism Prothymosin α/PTMA SREBP-1 STAT3 STAT3 Transcription Factor - metabolism Sterol Regulatory Element Binding Protein 1 - genetics Sterol Regulatory Element Binding Protein 1 - metabolism Thymosin - analogs & derivatives Thymosin - genetics Thymosin - metabolism Up-Regulation |
| title | Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation |
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