Overexpression of m(7)G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma

m(7)G 写入酶 METTL1 和 BUD23 的过表达赋予肾透明细胞癌致癌性

阅读:1

Abstract

Emerging evidence shows that N7-methylguanosine (m(7)G) modification and its writers contribute to the development of diverse cancers. However, the role of m(7)G writers in kidney renal clear cell carcinoma (KIRC) remains unclear. In this study we show that the catalytic components of m(7)G writers, METTL1 and BUD23, are overexpressed in advanced KIRC and are associated with worse overall survival. Knockdown of METTL1 or BUD23 inhibited cell proliferation, colony formation, and migration in KIRC cell lines, indicating their oncogenic role in KIRC. Furthermore, we observed that METTL1 and BUD23 expression was negatively correlated with the expression of key tumor suppressor genes commonly dysregulated in KIRC. We observed METTL1-mediated m(7)G methylation in mRNAs expressed by these tumor suppressor genes, indicating that METTL1 may regulate these genes via m(7)G modification. Overall, our study highlights the oncogenic role of METTL1 and BUD23 in KIRC and their potential as prognostic biomarkers and therapeutic targets in KIRC. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。