WTAP-Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non-Small Cell Lung Cancer by Regulating miR-612/CCL28 Axis
Accumulating evidence reveals that deregulated N6-methyladenosine (m A) RNA methylation and circular RNAs (circRNAs) are required for the tumorigenesis of non-small cell lung cancer (NSCLC). We aimed to uncover the underlying mechanisms by which WTAP-mediated m A modification of circRNA contributes...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2024-12, Vol.28 (23), p.e70207 |
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| creator | Zhu, Xun-Xia Chen, Xiao-Yu Zhao, Li-Ting Zhang, Xue-Lin Li, Yi-Ou Shen, Xiao-Yong |
| description | Accumulating evidence reveals that deregulated N6-methyladenosine (m
A) RNA methylation and circular RNAs (circRNAs) are required for the tumorigenesis of non-small cell lung cancer (NSCLC). We aimed to uncover the underlying mechanisms by which WTAP-mediated m
A modification of circRNA contributes to NSCLC. The differentially-expressed circRNAs were identified by a circRNA profiling microarray. The association of circSMOC1 with clinicopathological features and prognosis in patients with NSCLC was estimated by fluorescence in situ hybridization. WTAP-mediated m
A modification of circRNA was validated by RNA immunoprecipitation (RIP) and methylated RIP (MeRIP) assays. The role of circSMOC1 in NSCLC cells was validated by in vitro functional experiments and in vivo tumorigenesis models. CircSMOC1-specific binding with miR-612 was verified by RIP, luciferase gene report and RT-qPCR assays. The effect of circSMOC1 and/or miR-612 on CCL28 expression was detected by RT-qPCR and Western blotting analysis. We found that the expression levels of circSMOC1 were elevated in NSCLC tissues and associated with TNM stage and poor survival in patients with NSCLC. Knockdown of circSMOC1 impaired the tumorigenesis of NSCLC in vitro and in vivo, whereas restored expression of circSMOC1 displayed the opposite effect. Furthermore, WTAP was upregulated in NSCLC and mediated m
A modification of circSMOC1 and circSMOC1 abolished WTAP knockdown-caused tumour-suppressive effects. Then, circSMOC1 acted as a sponge of miR-612 to upregulate CCL28 and miR-612 inhibitors abrogated circSMOC1 knockdown-caused anti-proliferation effects and CCL28 downregulation in NSCLC cells. Knockdown of CCL28 inhibited cell proliferation and invasion and counteracted miR-612 inhibitor-caused tumour-promoting effects. Our findings unveil that WTAP-mediated m
A modification of circSMOC1 facilitates the tumorigenesis of NSCLC by regulating the miR-612/CCL28 axis. |
| doi_str_mv | 10.1111/jcmm.70207 |
| format | Article |
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A) RNA methylation and circular RNAs (circRNAs) are required for the tumorigenesis of non-small cell lung cancer (NSCLC). We aimed to uncover the underlying mechanisms by which WTAP-mediated m
A modification of circRNA contributes to NSCLC. The differentially-expressed circRNAs were identified by a circRNA profiling microarray. The association of circSMOC1 with clinicopathological features and prognosis in patients with NSCLC was estimated by fluorescence in situ hybridization. WTAP-mediated m
A modification of circRNA was validated by RNA immunoprecipitation (RIP) and methylated RIP (MeRIP) assays. The role of circSMOC1 in NSCLC cells was validated by in vitro functional experiments and in vivo tumorigenesis models. CircSMOC1-specific binding with miR-612 was verified by RIP, luciferase gene report and RT-qPCR assays. The effect of circSMOC1 and/or miR-612 on CCL28 expression was detected by RT-qPCR and Western blotting analysis. We found that the expression levels of circSMOC1 were elevated in NSCLC tissues and associated with TNM stage and poor survival in patients with NSCLC. Knockdown of circSMOC1 impaired the tumorigenesis of NSCLC in vitro and in vivo, whereas restored expression of circSMOC1 displayed the opposite effect. Furthermore, WTAP was upregulated in NSCLC and mediated m
A modification of circSMOC1 and circSMOC1 abolished WTAP knockdown-caused tumour-suppressive effects. Then, circSMOC1 acted as a sponge of miR-612 to upregulate CCL28 and miR-612 inhibitors abrogated circSMOC1 knockdown-caused anti-proliferation effects and CCL28 downregulation in NSCLC cells. Knockdown of CCL28 inhibited cell proliferation and invasion and counteracted miR-612 inhibitor-caused tumour-promoting effects. Our findings unveil that WTAP-mediated m
A modification of circSMOC1 facilitates the tumorigenesis of NSCLC by regulating the miR-612/CCL28 axis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.70207</identifier><identifier>PMID: 39632285</identifier><language>eng</language><publisher>England</publisher><subject>Adenosine - analogs & derivatives ; Adenosine - metabolism ; Animals ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Cycle Proteins ; Cell Line, Tumor ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Male ; Mice ; Mice, Nude ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Prognosis ; RNA Splicing Factors - genetics ; RNA Splicing Factors - metabolism ; RNA, Circular - genetics ; RNA, Circular - metabolism</subject><ispartof>Journal of cellular and molecular medicine, 2024-12, Vol.28 (23), p.e70207</ispartof><rights>2024 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c585-5a06e0f33fc91bec2b3833559acf76ceb55226a443015189f4ab5e20586006393</cites><orcidid>0000-0001-5922-2589</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39632285$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Xun-Xia</creatorcontrib><creatorcontrib>Chen, Xiao-Yu</creatorcontrib><creatorcontrib>Zhao, Li-Ting</creatorcontrib><creatorcontrib>Zhang, Xue-Lin</creatorcontrib><creatorcontrib>Li, Yi-Ou</creatorcontrib><creatorcontrib>Shen, Xiao-Yong</creatorcontrib><title>WTAP-Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non-Small Cell Lung Cancer by Regulating miR-612/CCL28 Axis</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Accumulating evidence reveals that deregulated N6-methyladenosine (m
A) RNA methylation and circular RNAs (circRNAs) are required for the tumorigenesis of non-small cell lung cancer (NSCLC). We aimed to uncover the underlying mechanisms by which WTAP-mediated m
A modification of circRNA contributes to NSCLC. The differentially-expressed circRNAs were identified by a circRNA profiling microarray. The association of circSMOC1 with clinicopathological features and prognosis in patients with NSCLC was estimated by fluorescence in situ hybridization. WTAP-mediated m
A modification of circRNA was validated by RNA immunoprecipitation (RIP) and methylated RIP (MeRIP) assays. The role of circSMOC1 in NSCLC cells was validated by in vitro functional experiments and in vivo tumorigenesis models. CircSMOC1-specific binding with miR-612 was verified by RIP, luciferase gene report and RT-qPCR assays. The effect of circSMOC1 and/or miR-612 on CCL28 expression was detected by RT-qPCR and Western blotting analysis. We found that the expression levels of circSMOC1 were elevated in NSCLC tissues and associated with TNM stage and poor survival in patients with NSCLC. Knockdown of circSMOC1 impaired the tumorigenesis of NSCLC in vitro and in vivo, whereas restored expression of circSMOC1 displayed the opposite effect. Furthermore, WTAP was upregulated in NSCLC and mediated m
A modification of circSMOC1 and circSMOC1 abolished WTAP knockdown-caused tumour-suppressive effects. Then, circSMOC1 acted as a sponge of miR-612 to upregulate CCL28 and miR-612 inhibitors abrogated circSMOC1 knockdown-caused anti-proliferation effects and CCL28 downregulation in NSCLC cells. Knockdown of CCL28 inhibited cell proliferation and invasion and counteracted miR-612 inhibitor-caused tumour-promoting effects. Our findings unveil that WTAP-mediated m
A modification of circSMOC1 facilitates the tumorigenesis of NSCLC by regulating the miR-612/CCL28 axis.</description><subject>Adenosine - analogs & derivatives</subject><subject>Adenosine - metabolism</subject><subject>Animals</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Cycle Proteins</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Prognosis</subject><subject>RNA Splicing Factors - genetics</subject><subject>RNA Splicing Factors - metabolism</subject><subject>RNA, Circular - genetics</subject><subject>RNA, Circular - metabolism</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMtKw0AUhgdRrFY3PoDMWkg7l8x0sgzBG6RW2oDLMJmc1Cm5lJkG7Cv41Ka2ehbn_Bw-_sWH0B0lEzrMdGOaZjIjjMzO0BUVigVhxMPzU6aKqxG69n5DCJeUR5doxCPJGVPiCn1_ZPF7MIfS6h2UuMESx3jelbayRu9s1-KuwsY6s5ovEopjY6AGN7Ae7z4BZ33TObuGFrz1B_Sta4NVo-saJzCstG_XONGtAYeLPV7Cuq-H2uHZ2GUgKZsmScoUjr-sv0EXla493J7uGGVPj1nyEqSL59ckTgMjlAiEJhJIxXllIlqAYQVXnAsRaVPNpIFCCMakDkNOqKAqqkJdCGBEKEmI5BEfo4djrXGd9w6qfOtso90-pyQ_-MwPPvNfnwN8f4S3fdFA-Y_-CeQ_aVduWQ</recordid><startdate>202412</startdate><enddate>202412</enddate><creator>Zhu, Xun-Xia</creator><creator>Chen, Xiao-Yu</creator><creator>Zhao, Li-Ting</creator><creator>Zhang, Xue-Lin</creator><creator>Li, Yi-Ou</creator><creator>Shen, Xiao-Yong</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0001-5922-2589</orcidid></search><sort><creationdate>202412</creationdate><title>WTAP-Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non-Small Cell Lung Cancer by Regulating miR-612/CCL28 Axis</title><author>Zhu, Xun-Xia ; Chen, Xiao-Yu ; Zhao, Li-Ting ; Zhang, Xue-Lin ; Li, Yi-Ou ; Shen, Xiao-Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c585-5a06e0f33fc91bec2b3833559acf76ceb55226a443015189f4ab5e20586006393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adenosine - analogs & derivatives</topic><topic>Adenosine - metabolism</topic><topic>Animals</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Cycle Proteins</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Prognosis</topic><topic>RNA Splicing Factors - genetics</topic><topic>RNA Splicing Factors - metabolism</topic><topic>RNA, Circular - genetics</topic><topic>RNA, Circular - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Xun-Xia</creatorcontrib><creatorcontrib>Chen, Xiao-Yu</creatorcontrib><creatorcontrib>Zhao, Li-Ting</creatorcontrib><creatorcontrib>Zhang, Xue-Lin</creatorcontrib><creatorcontrib>Li, Yi-Ou</creatorcontrib><creatorcontrib>Shen, Xiao-Yong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Xun-Xia</au><au>Chen, Xiao-Yu</au><au>Zhao, Li-Ting</au><au>Zhang, Xue-Lin</au><au>Li, Yi-Ou</au><au>Shen, Xiao-Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>WTAP-Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non-Small Cell Lung Cancer by Regulating miR-612/CCL28 Axis</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2024-12</date><risdate>2024</risdate><volume>28</volume><issue>23</issue><spage>e70207</spage><pages>e70207-</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Accumulating evidence reveals that deregulated N6-methyladenosine (m
A) RNA methylation and circular RNAs (circRNAs) are required for the tumorigenesis of non-small cell lung cancer (NSCLC). We aimed to uncover the underlying mechanisms by which WTAP-mediated m
A modification of circRNA contributes to NSCLC. The differentially-expressed circRNAs were identified by a circRNA profiling microarray. The association of circSMOC1 with clinicopathological features and prognosis in patients with NSCLC was estimated by fluorescence in situ hybridization. WTAP-mediated m
A modification of circRNA was validated by RNA immunoprecipitation (RIP) and methylated RIP (MeRIP) assays. The role of circSMOC1 in NSCLC cells was validated by in vitro functional experiments and in vivo tumorigenesis models. CircSMOC1-specific binding with miR-612 was verified by RIP, luciferase gene report and RT-qPCR assays. The effect of circSMOC1 and/or miR-612 on CCL28 expression was detected by RT-qPCR and Western blotting analysis. We found that the expression levels of circSMOC1 were elevated in NSCLC tissues and associated with TNM stage and poor survival in patients with NSCLC. Knockdown of circSMOC1 impaired the tumorigenesis of NSCLC in vitro and in vivo, whereas restored expression of circSMOC1 displayed the opposite effect. Furthermore, WTAP was upregulated in NSCLC and mediated m
A modification of circSMOC1 and circSMOC1 abolished WTAP knockdown-caused tumour-suppressive effects. Then, circSMOC1 acted as a sponge of miR-612 to upregulate CCL28 and miR-612 inhibitors abrogated circSMOC1 knockdown-caused anti-proliferation effects and CCL28 downregulation in NSCLC cells. Knockdown of CCL28 inhibited cell proliferation and invasion and counteracted miR-612 inhibitor-caused tumour-promoting effects. Our findings unveil that WTAP-mediated m
A modification of circSMOC1 facilitates the tumorigenesis of NSCLC by regulating the miR-612/CCL28 axis.</abstract><cop>England</cop><pmid>39632285</pmid><doi>10.1111/jcmm.70207</doi><orcidid>https://orcid.org/0000-0001-5922-2589</orcidid></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Online Library Open Access; PubMed Central |
| subjects | Adenosine - analogs & derivatives Adenosine - metabolism Animals Carcinogenesis - genetics Carcinogenesis - pathology Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Cycle Proteins Cell Line, Tumor Cell Proliferation - genetics Female Gene Expression Regulation, Neoplastic Humans Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Male Mice Mice, Nude MicroRNAs - genetics MicroRNAs - metabolism Middle Aged Prognosis RNA Splicing Factors - genetics RNA Splicing Factors - metabolism RNA, Circular - genetics RNA, Circular - metabolism |
| title | WTAP-Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non-Small Cell Lung Cancer by Regulating miR-612/CCL28 Axis |
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