{"title":"fto介导的KCTD11 RNA低甲基化促进非小细胞肺癌的进展","authors":"Xin Liu, Bing Bai, Li Wei, Zhengchang Song","doi":"10.1615/CritRevEukaryotGeneExpr.2025059017","DOIUrl":null,"url":null,"abstract":"<p><p>N6-methyladenosine (m6A) plays a role in tumorigenesis of lung cancer (NSCLC); FTO functions as an oncogene in various cancers. However, the molecular mechanism underlying FTO-promoted lung cancer progression is still unclear. Gene expression was detected using RT-qPCR, western blot, and immunohistochemistry. The behaviors of lung cancer cells were detected using CCK-8, colony formation assay, and transwell assays. MeRIP and luciferase assays were conducted to FTO-mediated RNA hypomethylation. In vivo assays were performed to verify the roles of FTO in NSCLC. High levels of FTO in NSCLC patients predicted poor outcomes. However, FTO knockdown suppressed the proliferation and migration of A549 cells. Mechanically, FTO downregulated KCTD11 expression through promoting the RNA hypomethylation of KCTD11, the expression of which was decreased in NSCLC. KCTD11 knockdown attenuated the effects of FTO and promoted the malignancy of lung cancer. In summary, FTO functions as an oncogene in NSCLC via downregulating KCTD11. Therefore, FTO/KCTD11 can be a novel target for NSCLC.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 6","pages":"15-25"},"PeriodicalIF":1.6000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"FTO-Mediated RNA Hypomethylation of KCTD11 Promotes the Progression of Non-Small Cell Lung Cancer.\",\"authors\":\"Xin Liu, Bing Bai, Li Wei, Zhengchang Song\",\"doi\":\"10.1615/CritRevEukaryotGeneExpr.2025059017\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>N6-methyladenosine (m6A) plays a role in tumorigenesis of lung cancer (NSCLC); FTO functions as an oncogene in various cancers. However, the molecular mechanism underlying FTO-promoted lung cancer progression is still unclear. Gene expression was detected using RT-qPCR, western blot, and immunohistochemistry. The behaviors of lung cancer cells were detected using CCK-8, colony formation assay, and transwell assays. MeRIP and luciferase assays were conducted to FTO-mediated RNA hypomethylation. In vivo assays were performed to verify the roles of FTO in NSCLC. High levels of FTO in NSCLC patients predicted poor outcomes. However, FTO knockdown suppressed the proliferation and migration of A549 cells. Mechanically, FTO downregulated KCTD11 expression through promoting the RNA hypomethylation of KCTD11, the expression of which was decreased in NSCLC. KCTD11 knockdown attenuated the effects of FTO and promoted the malignancy of lung cancer. In summary, FTO functions as an oncogene in NSCLC via downregulating KCTD11. Therefore, FTO/KCTD11 can be a novel target for NSCLC.</p>\",\"PeriodicalId\":56317,\"journal\":{\"name\":\"Critical Reviews in Eukaryotic Gene Expression\",\"volume\":\"35 6\",\"pages\":\"15-25\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Critical Reviews in Eukaryotic Gene Expression\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025059017\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Critical Reviews in Eukaryotic Gene Expression","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025059017","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
FTO-Mediated RNA Hypomethylation of KCTD11 Promotes the Progression of Non-Small Cell Lung Cancer.
N6-methyladenosine (m6A) plays a role in tumorigenesis of lung cancer (NSCLC); FTO functions as an oncogene in various cancers. However, the molecular mechanism underlying FTO-promoted lung cancer progression is still unclear. Gene expression was detected using RT-qPCR, western blot, and immunohistochemistry. The behaviors of lung cancer cells were detected using CCK-8, colony formation assay, and transwell assays. MeRIP and luciferase assays were conducted to FTO-mediated RNA hypomethylation. In vivo assays were performed to verify the roles of FTO in NSCLC. High levels of FTO in NSCLC patients predicted poor outcomes. However, FTO knockdown suppressed the proliferation and migration of A549 cells. Mechanically, FTO downregulated KCTD11 expression through promoting the RNA hypomethylation of KCTD11, the expression of which was decreased in NSCLC. KCTD11 knockdown attenuated the effects of FTO and promoted the malignancy of lung cancer. In summary, FTO functions as an oncogene in NSCLC via downregulating KCTD11. Therefore, FTO/KCTD11 can be a novel target for NSCLC.
期刊介绍：
Critical ReviewsTM in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our mechanistic understanding of gene regulation, organization, and structure within the contexts of biological control and the diagnosis/treatment of disease. The journal provides in-depth critical reviews, on well-defined topics of immediate interest, written by recognized specialists in the field. Extensive literature citations provide a comprehensive information resource.
Reviews are developed from an historical perspective and suggest directions that can be anticipated. Strengths as well as limitations of methodologies and experimental strategies are considered.
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