USF1 regulated circPRDM4 modulates tumorigenesis and immune escape in chemoresistant cervical cancer
Cervical cancer (CC) represents a major global health concern, characterized by chemoresistance and immune evasion mechanisms. Circular RNAs (circRNAs), which play a crucial role in cancer pathogenesis, particularly in the case of CC, have gained significant attention. The primary objective of this...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2024-03, Vol.28 (5), p.e17945-n/a |
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| creator | Zhang, Yan Li, Xing Zhang, Jun Mao, Lin Wen, Zou Cao, Mingliang Mu, Xuefeng |
| description | Cervical cancer (CC) represents a major global health concern, characterized by chemoresistance and immune evasion mechanisms. Circular RNAs (circRNAs), which play a crucial role in cancer pathogenesis, particularly in the case of CC, have gained significant attention. The primary objective of this study was to investigate the functional significance of circRNAs in chemoresistant CC. A significant upregulation of circPRDM4 expression in chemoresistant CC cells. To investigate the functional consequences, we conducted circPRDM4 knockdown experiments, which resulted in the effective blockade of immune escape mechanisms employed by chemoresistant CC cells. Furthermore, circPRDM4 knockdown demonstrated a significant suppression of tumorigenesis in CC cells, highlighting its contribution to the oncogenic potential of CC. Investigating the regulatory mechanisms involved, we found that the transcriptional factor upstream stimulatory factor 1 (USF1) acts as an inducer of circPRDM4 expression. Remarkably, USF1 was found to effectively modulate CC cell immune escape via its interaction with circPRDM4. Moreover, our results revealed that USF1 is intricately involved in CC cell tumorigenesis through the regulation of circPRDM4. Collectively, our study elucidates the significant roles of circPRDM4 and its upstream regulator USF1 in chemoresistant CC cells. These findings underscore the importance of circRNAs in CC pathogenesis and provide valuable insights into the mechanisms underlying immune escape and tumorigenesis. |
| doi_str_mv | 10.1111/jcmm.17945 |
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Circular RNAs (circRNAs), which play a crucial role in cancer pathogenesis, particularly in the case of CC, have gained significant attention. The primary objective of this study was to investigate the functional significance of circRNAs in chemoresistant CC. A significant upregulation of circPRDM4 expression in chemoresistant CC cells. To investigate the functional consequences, we conducted circPRDM4 knockdown experiments, which resulted in the effective blockade of immune escape mechanisms employed by chemoresistant CC cells. Furthermore, circPRDM4 knockdown demonstrated a significant suppression of tumorigenesis in CC cells, highlighting its contribution to the oncogenic potential of CC. Investigating the regulatory mechanisms involved, we found that the transcriptional factor upstream stimulatory factor 1 (USF1) acts as an inducer of circPRDM4 expression. Remarkably, USF1 was found to effectively modulate CC cell immune escape via its interaction with circPRDM4. Moreover, our results revealed that USF1 is intricately involved in CC cell tumorigenesis through the regulation of circPRDM4. Collectively, our study elucidates the significant roles of circPRDM4 and its upstream regulator USF1 in chemoresistant CC cells. These findings underscore the importance of circRNAs in CC pathogenesis and provide valuable insights into the mechanisms underlying immune escape and tumorigenesis.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17945</identifier><identifier>PMID: 37665075</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Antibodies ; Cell growth ; Cervical cancer ; Chemoresistance ; Chemotherapy ; circPRDM4 ; Circular RNA ; Enzymes ; immune escape ; Immune evasion ; Metastasis ; MicroRNAs ; Original ; Pathogenesis ; Public health ; Reagents ; Software ; Tumor necrosis factor-TNF ; Tumorigenesis ; Upstream stimulating factor 1 ; USF1</subject><ispartof>Journal of cellular and molecular medicine, 2024-03, Vol.28 (5), p.e17945-n/a</ispartof><rights>2023 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4625-4cbbf749b65692496c331ec114ccdebe9707053976ce1dd8d2b4c6f48c1af6cc3</cites><orcidid>0009-0008-5997-2724</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10902569/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10902569/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46030,46454,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37665075$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Li, Xing</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Mao, Lin</creatorcontrib><creatorcontrib>Wen, Zou</creatorcontrib><creatorcontrib>Cao, Mingliang</creatorcontrib><creatorcontrib>Mu, Xuefeng</creatorcontrib><title>USF1 regulated circPRDM4 modulates tumorigenesis and immune escape in chemoresistant cervical cancer</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Cervical cancer (CC) represents a major global health concern, characterized by chemoresistance and immune evasion mechanisms. Circular RNAs (circRNAs), which play a crucial role in cancer pathogenesis, particularly in the case of CC, have gained significant attention. The primary objective of this study was to investigate the functional significance of circRNAs in chemoresistant CC. A significant upregulation of circPRDM4 expression in chemoresistant CC cells. To investigate the functional consequences, we conducted circPRDM4 knockdown experiments, which resulted in the effective blockade of immune escape mechanisms employed by chemoresistant CC cells. Furthermore, circPRDM4 knockdown demonstrated a significant suppression of tumorigenesis in CC cells, highlighting its contribution to the oncogenic potential of CC. Investigating the regulatory mechanisms involved, we found that the transcriptional factor upstream stimulatory factor 1 (USF1) acts as an inducer of circPRDM4 expression. Remarkably, USF1 was found to effectively modulate CC cell immune escape via its interaction with circPRDM4. Moreover, our results revealed that USF1 is intricately involved in CC cell tumorigenesis through the regulation of circPRDM4. Collectively, our study elucidates the significant roles of circPRDM4 and its upstream regulator USF1 in chemoresistant CC cells. These findings underscore the importance of circRNAs in CC pathogenesis and provide valuable insights into the mechanisms underlying immune escape and tumorigenesis.</description><subject>Antibodies</subject><subject>Cell growth</subject><subject>Cervical cancer</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>circPRDM4</subject><subject>Circular RNA</subject><subject>Enzymes</subject><subject>immune escape</subject><subject>Immune evasion</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>Original</subject><subject>Pathogenesis</subject><subject>Public health</subject><subject>Reagents</subject><subject>Software</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumorigenesis</subject><subject>Upstream stimulating factor 1</subject><subject>USF1</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU1v1DAQhi1ERUvhwg9AlrggpC3-ihOfEFooFHUFAnq2nMlk61XsLHZS1H-Pt7tUwAFfPPI8ejz2S8gzzs54Wa83EMIZr42qHpATXjVioYxUDw81b2RzTB7nvGFMai7NI3Isa60rVlcnpLv6ds5pwvU8uAk7Cj7Bl6_vVoqGsbs7y3Saw5j8GiNmn6mLHfUhzBEpZnBbpD5SuMbC7PqTixMFTDce3EDBxVI_IUe9GzI-Peyn5Or8_fflx8Xl5w8Xy7eXC1BaVAsFbdvXyrS60kYoo0FKjsC5AuiwRVOzmlXS1BqQd13TiVaB7lUD3PUaQJ6SN3vvdm4DdoBxSm6w2-SDS7d2dN7-3Yn-2q7HG8uZYaJcWgwvD4Y0_pgxTzb4DDgMLuI4ZysazTQvP60K-uIfdDPOKZb3WWGkaIRRUhbq1Z6CNOacsL-fhjO7S8_u0rN36RX4-Z_z36O_4yoA3wM__YC3_1HZT8vVai_9BdMCpsc</recordid><startdate>202403</startdate><enddate>202403</enddate><creator>Zhang, Yan</creator><creator>Li, Xing</creator><creator>Zhang, Jun</creator><creator>Mao, Lin</creator><creator>Wen, Zou</creator><creator>Cao, Mingliang</creator><creator>Mu, Xuefeng</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0009-0008-5997-2724</orcidid></search><sort><creationdate>202403</creationdate><title>USF1 regulated circPRDM4 modulates tumorigenesis and immune escape in chemoresistant cervical cancer</title><author>Zhang, Yan ; Li, Xing ; Zhang, Jun ; Mao, Lin ; Wen, Zou ; Cao, Mingliang ; Mu, Xuefeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4625-4cbbf749b65692496c331ec114ccdebe9707053976ce1dd8d2b4c6f48c1af6cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antibodies</topic><topic>Cell growth</topic><topic>Cervical cancer</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>circPRDM4</topic><topic>Circular RNA</topic><topic>Enzymes</topic><topic>immune escape</topic><topic>Immune evasion</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>Original</topic><topic>Pathogenesis</topic><topic>Public health</topic><topic>Reagents</topic><topic>Software</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumorigenesis</topic><topic>Upstream stimulating factor 1</topic><topic>USF1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Li, Xing</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Mao, Lin</creatorcontrib><creatorcontrib>Wen, Zou</creatorcontrib><creatorcontrib>Cao, Mingliang</creatorcontrib><creatorcontrib>Mu, Xuefeng</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yan</au><au>Li, Xing</au><au>Zhang, Jun</au><au>Mao, Lin</au><au>Wen, Zou</au><au>Cao, Mingliang</au><au>Mu, Xuefeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>USF1 regulated circPRDM4 modulates tumorigenesis and immune escape in chemoresistant cervical cancer</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2024-03</date><risdate>2024</risdate><volume>28</volume><issue>5</issue><spage>e17945</spage><epage>n/a</epage><pages>e17945-n/a</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Cervical cancer (CC) represents a major global health concern, characterized by chemoresistance and immune evasion mechanisms. Circular RNAs (circRNAs), which play a crucial role in cancer pathogenesis, particularly in the case of CC, have gained significant attention. The primary objective of this study was to investigate the functional significance of circRNAs in chemoresistant CC. A significant upregulation of circPRDM4 expression in chemoresistant CC cells. To investigate the functional consequences, we conducted circPRDM4 knockdown experiments, which resulted in the effective blockade of immune escape mechanisms employed by chemoresistant CC cells. Furthermore, circPRDM4 knockdown demonstrated a significant suppression of tumorigenesis in CC cells, highlighting its contribution to the oncogenic potential of CC. Investigating the regulatory mechanisms involved, we found that the transcriptional factor upstream stimulatory factor 1 (USF1) acts as an inducer of circPRDM4 expression. Remarkably, USF1 was found to effectively modulate CC cell immune escape via its interaction with circPRDM4. Moreover, our results revealed that USF1 is intricately involved in CC cell tumorigenesis through the regulation of circPRDM4. Collectively, our study elucidates the significant roles of circPRDM4 and its upstream regulator USF1 in chemoresistant CC cells. These findings underscore the importance of circRNAs in CC pathogenesis and provide valuable insights into the mechanisms underlying immune escape and tumorigenesis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>37665075</pmid><doi>10.1111/jcmm.17945</doi><tpages>10</tpages><orcidid>https://orcid.org/0009-0008-5997-2724</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Cell growth Cervical cancer Chemoresistance Chemotherapy circPRDM4 Circular RNA Enzymes immune escape Immune evasion Metastasis MicroRNAs Original Pathogenesis Public health Reagents Software Tumor necrosis factor-TNF Tumorigenesis Upstream stimulating factor 1 USF1 |
| title | USF1 regulated circPRDM4 modulates tumorigenesis and immune escape in chemoresistant cervical cancer |
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