被撤回的出版物: Methyltransferase-like 1 (METTL1) served as a tumor suppressor in colon cancer by activating 7-methyguanosine (m7G) regulated let-7e miRNA/HMGA2 axis (Retracted article. See vol. 306, 2022)
[摘要] Aims: This study aimed to uncover the underlying mechanisms of METTL1/let-7e miRNA/HMGA2 axis regulated colon cancer (CC) development. Materials and methods: Real-Time qPCR was used to detect the expression levels of METTL1 mRNA and let-7e miRNA in clinical specimens and cell lines. Pearson correlation analysis was conducted to analyze the correlation of let-7e miRNA and METTL1 mRNA in cancer tissues. Western Blot was performed to examine protein expressions. Cell proliferation was evaluated by CCK-8 assay and cell mobility was determined by transwell assay. Dual-luciferase reporter gene system was used to validate the binding sites of let-7e miRNA and 3' UTR regions of HMGA2 mRNA. Key findings: METTL1 and let-7e miRNA were low-expressed in CC tissues and cells compared to their normal counterparts. Overexpression of METTL1 inhibited CC cell proliferation, invasion as well as migration, and promoted cell apoptosis. Further results validated that METTL1 overexpression increased the levels of let-7e miRNA in CC cell lines, and the effects of overexpressed METTL1 on the above cell functions were reversed by knocking down let-7e miRNA. In addition, high mobility group AT-hook 2 (HMGA2) was the downstream target of let-7e miRNA, and overexpressed METTL1 inhibited HMGA2 expressions by upregulating let-7e miRNA in CC cells. Interestingly, the effects of overexpressed METTL1 on CC cell functions were also reversed by upregulating HMGA2. Significance: Overexpression of METTL1 inhibited CC progression by inhibiting HMGA2 through upregulating let-7e miRNA.
[发布日期] 2020-05-15 [发布机构]
[效力级别] Retracted Publication [学科分类]
[关键词] Methyltransferase-like 1;7-methyguanosine;Colon cancer;Let-7e miRNA;HMGA2 [时效性]