{"title":"WTAP敲低通过调节SNAIL1在结直肠癌中的表达抑制细胞迁移。","authors":"Jingjing Han, Jiankun Zhang, Huilong Shi, Xiaowen Wen","doi":"10.62347/QAQE4354","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>N6-methyladenosine (m6A) modification is the most prevalent mRNA modification in carcinogenesis and it plays a crucial role. WTAP, an m6A RNA methyltransferase, is functionally significant in various cancers; however, the specific role and functional mechanism in colorectal cancer (CRC) remain poorly understood.</p><p><strong>Method: </strong>In this study, we utilized Gene Expression Profiling Interactive Analysis (GEPIA) to compare WTAP expression in CRC and normal tissues. Functional assays including colony formation assay and transwell assay were conducted to assess the impact of WTAP on cell viability and migration. RNA dot blot and MeRIP-PCR assays were used to investigate WTAP's role in m6A modification.</p><p><strong>Results: </strong>WTAP expression was elevated in CRC tissues. Colony formation and transwell assays showed that WTAP promoted proliferation and migration of CRC cells in vitro. Mechanistically, MeRIP-PCR analysis demonstrated that WTAP knockdown inhibited SNAI1 expression by reducing m6A modification of SNAI1 in CRC cells. Supporting this, analysis of data from GEPIA and cBioPortal revealed a positive correlation between WTAP and SNAI1 expression.</p><p><strong>Conclusion: </strong>WTAP may act as an oncogene in CRC by regulating SNAI1 expression.</p>","PeriodicalId":7731,"journal":{"name":"American journal of translational research","volume":"16 12","pages":"8023-8031"},"PeriodicalIF":1.7000,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733317/pdf/","citationCount":"0","resultStr":"{\"title\":\"WTAP knockdown inhibits cell migration through regulating SNAIL1 expression in colorectal cancer.\",\"authors\":\"Jingjing Han, Jiankun Zhang, Huilong Shi, Xiaowen Wen\",\"doi\":\"10.62347/QAQE4354\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>N6-methyladenosine (m6A) modification is the most prevalent mRNA modification in carcinogenesis and it plays a crucial role. WTAP, an m6A RNA methyltransferase, is functionally significant in various cancers; however, the specific role and functional mechanism in colorectal cancer (CRC) remain poorly understood.</p><p><strong>Method: </strong>In this study, we utilized Gene Expression Profiling Interactive Analysis (GEPIA) to compare WTAP expression in CRC and normal tissues. Functional assays including colony formation assay and transwell assay were conducted to assess the impact of WTAP on cell viability and migration. RNA dot blot and MeRIP-PCR assays were used to investigate WTAP's role in m6A modification.</p><p><strong>Results: </strong>WTAP expression was elevated in CRC tissues. Colony formation and transwell assays showed that WTAP promoted proliferation and migration of CRC cells in vitro. Mechanistically, MeRIP-PCR analysis demonstrated that WTAP knockdown inhibited SNAI1 expression by reducing m6A modification of SNAI1 in CRC cells. Supporting this, analysis of data from GEPIA and cBioPortal revealed a positive correlation between WTAP and SNAI1 expression.</p><p><strong>Conclusion: </strong>WTAP may act as an oncogene in CRC by regulating SNAI1 expression.</p>\",\"PeriodicalId\":7731,\"journal\":{\"name\":\"American journal of translational research\",\"volume\":\"16 12\",\"pages\":\"8023-8031\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-12-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733317/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of translational research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/QAQE4354\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of translational research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/QAQE4354","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
WTAP knockdown inhibits cell migration through regulating SNAIL1 expression in colorectal cancer.
Objective: N6-methyladenosine (m6A) modification is the most prevalent mRNA modification in carcinogenesis and it plays a crucial role. WTAP, an m6A RNA methyltransferase, is functionally significant in various cancers; however, the specific role and functional mechanism in colorectal cancer (CRC) remain poorly understood.
Method: In this study, we utilized Gene Expression Profiling Interactive Analysis (GEPIA) to compare WTAP expression in CRC and normal tissues. Functional assays including colony formation assay and transwell assay were conducted to assess the impact of WTAP on cell viability and migration. RNA dot blot and MeRIP-PCR assays were used to investigate WTAP's role in m6A modification.
Results: WTAP expression was elevated in CRC tissues. Colony formation and transwell assays showed that WTAP promoted proliferation and migration of CRC cells in vitro. Mechanistically, MeRIP-PCR analysis demonstrated that WTAP knockdown inhibited SNAI1 expression by reducing m6A modification of SNAI1 in CRC cells. Supporting this, analysis of data from GEPIA and cBioPortal revealed a positive correlation between WTAP and SNAI1 expression.
Conclusion: WTAP may act as an oncogene in CRC by regulating SNAI1 expression.