TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer
Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radioth...
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| Veröffentlicht in: | Oncogene 2022-03, Vol.41 (11), p.1589-1599 |
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| creator | Ma, Yan Zhang, Haibo Chen, Cheng Liu, Lixin Ding, Ting Wang, Ying Ma, Dachang Ling, Xiaoling Chen, Xiaohua Li, Jianping Guansheng Zhong Ru, Guoqing Zhang, Lei Tang, Jianming |
| description | Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients. |
| doi_str_mv | 10.1038/s41388-022-02204-1 |
| format | Article |
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Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-022-02204-1</identifier><identifier>PMID: 35091679</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/95 ; 38/77 ; 631/67/1059/485 ; 631/67/1347 ; 64/60 ; Apoptosis ; Breast cancer ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation ; Dephosphorylation ; Gene Expression Regulation, Neoplastic ; Human Genetics ; Humans ; Internal Medicine ; Medical prognosis ; Medicine ; Medicine & Public Health ; Molecular modelling ; Oncology ; Patients ; Phosphorylation ; Radiation therapy ; Radioresistance ; Stat3 protein ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; Transcription activation ; Transcription Factors - metabolism ; Transcriptional Activation ; Tripartite Motif Proteins - metabolism ; Triple Negative Breast Neoplasms - genetics ; Triple Negative Breast Neoplasms - metabolism ; Triple Negative Breast Neoplasms - radiotherapy ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Oncogene, 2022-03, Vol.41 (11), p.1589-1599</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature Limited.</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-f48c0c0bdb07a7331178abd3014f0fddbb6f0542c35346f25c4eb7a92a80fc0c3</citedby><cites>FETCH-LOGICAL-c375t-f48c0c0bdb07a7331178abd3014f0fddbb6f0542c35346f25c4eb7a92a80fc0c3</cites><orcidid>0000-0003-3738-9761</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-022-02204-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-022-02204-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35091679$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Yan</creatorcontrib><creatorcontrib>Zhang, Haibo</creatorcontrib><creatorcontrib>Chen, Cheng</creatorcontrib><creatorcontrib>Liu, Lixin</creatorcontrib><creatorcontrib>Ding, Ting</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Ma, Dachang</creatorcontrib><creatorcontrib>Ling, Xiaoling</creatorcontrib><creatorcontrib>Chen, Xiaohua</creatorcontrib><creatorcontrib>Li, Jianping</creatorcontrib><creatorcontrib>Guansheng</creatorcontrib><creatorcontrib>Zhong</creatorcontrib><creatorcontrib>Ru, Guoqing</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Tang, Jianming</creatorcontrib><title>TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients.</description><subject>13/1</subject><subject>13/95</subject><subject>38/77</subject><subject>631/67/1059/485</subject><subject>631/67/1347</subject><subject>64/60</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Dephosphorylation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular modelling</subject><subject>Oncology</subject><subject>Patients</subject><subject>Phosphorylation</subject><subject>Radiation therapy</subject><subject>Radioresistance</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Transcription activation</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptional Activation</subject><subject>Tripartite Motif Proteins - metabolism</subject><subject>Triple Negative Breast Neoplasms - genetics</subject><subject>Triple Negative Breast Neoplasms - metabolism</subject><subject>Triple Negative Breast Neoplasms - radiotherapy</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtr3DAUhUVJ6Uwef6CLYMgmG7VXL0tahiFpAymF1l0LWZYHDTP2RJID-ffV1NMEsshCXIG-c-7VPQh9JvCFAFNfEydMKQyUHg5wTD6gJeGyxkJofoKWoAVgTRldoNOUNgAgNdBPaMEEaFJLvUS--XX_g9FqH8fdmH2qou3CGH0KKdvB-ap9rrqQ4rTPYVhXzYoL_Lu5aVgVhuyjdTmMQ7lXOYb91uPBr20OT0UXvU25cgeTeI4-9nab_MWxnqE_d7fN6jt--PntfnXzgB2TIuOeKwcO2q4FaSVjhEhl244B4T30Xde2dQ-CU8cE43VPheO-lVZTq6AvSnaGrmff8p3HyadsdiE5v93awY9TMrSmTGmqhSzo1Rt0M05xKNMViklFaqp0oehMuTimFH1v9jHsbHw2BMwhBDOHYEoA5l8IhhTR5dF6ane-e5H833oB2Ayk8jSsfXzt_Y7tX_2TkZs</recordid><startdate>20220310</startdate><enddate>20220310</enddate><creator>Ma, Yan</creator><creator>Zhang, Haibo</creator><creator>Chen, Cheng</creator><creator>Liu, Lixin</creator><creator>Ding, Ting</creator><creator>Wang, Ying</creator><creator>Ma, Dachang</creator><creator>Ling, Xiaoling</creator><creator>Chen, Xiaohua</creator><creator>Li, Jianping</creator><creator>Guansheng</creator><creator>Zhong</creator><creator>Ru, Guoqing</creator><creator>Zhang, Lei</creator><creator>Tang, Jianming</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3738-9761</orcidid></search><sort><creationdate>20220310</creationdate><title>TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer</title><author>Ma, Yan ; Zhang, Haibo ; Chen, Cheng ; Liu, Lixin ; Ding, Ting ; Wang, Ying ; Ma, Dachang ; Ling, Xiaoling ; Chen, Xiaohua ; Li, Jianping ; Guansheng ; Zhong ; Ru, Guoqing ; Zhang, Lei ; Tang, Jianming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-f48c0c0bdb07a7331178abd3014f0fddbb6f0542c35346f25c4eb7a92a80fc0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>13/1</topic><topic>13/95</topic><topic>38/77</topic><topic>631/67/1059/485</topic><topic>631/67/1347</topic><topic>64/60</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Dephosphorylation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular modelling</topic><topic>Oncology</topic><topic>Patients</topic><topic>Phosphorylation</topic><topic>Radiation therapy</topic><topic>Radioresistance</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Yan</au><au>Zhang, Haibo</au><au>Chen, Cheng</au><au>Liu, Lixin</au><au>Ding, Ting</au><au>Wang, Ying</au><au>Ma, Dachang</au><au>Ling, Xiaoling</au><au>Chen, Xiaohua</au><au>Li, Jianping</au><au>Guansheng</au><au>Zhong</au><au>Ru, Guoqing</au><au>Zhang, Lei</au><au>Tang, Jianming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2022-03-10</date><risdate>2022</risdate><volume>41</volume><issue>11</issue><spage>1589</spage><epage>1599</epage><pages>1589-1599</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>35091679</pmid><doi>10.1038/s41388-022-02204-1</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-3738-9761</orcidid></addata></record> |
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| subjects | 13/1 13/95 38/77 631/67/1059/485 631/67/1347 64/60 Apoptosis Breast cancer Cell Biology Cell Line, Tumor Cell Proliferation Dephosphorylation Gene Expression Regulation, Neoplastic Human Genetics Humans Internal Medicine Medical prognosis Medicine Medicine & Public Health Molecular modelling Oncology Patients Phosphorylation Radiation therapy Radioresistance Stat3 protein STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Transcription activation Transcription Factors - metabolism Transcriptional Activation Tripartite Motif Proteins - metabolism Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - metabolism Triple Negative Breast Neoplasms - radiotherapy Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism |
| title | TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer |
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