FTO通过依赖于mA的途径上调PDK1，促进透明细胞肾细胞癌进展。

FTO promotes clear cell renal cell carcinoma progression via upregulation of PDK1 through an mA dependent pathway.

作者信息

Shen Haixiang, Ying Yufan, Ma Xueyou, Xie Haiyun, Chen Shiming, Sun Jiazhu, Liu Zixiang, Wen Chao, Yang Zitong, Wang Xiao, Xu Mingjie, Luo Jindan, Liu Ben, Li Jiangfeng, Zheng Xiangyi, Xie Liping

机构信息

Department of Urology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, Zhejiang, China.

Cancer Center, Zhejiang University, Hangzhou, 310058, Zhejiang, China.

出版信息

Cell Death Discov. 2022 Aug 12;8(1):356. doi: 10.1038/s41420-022-01151-w.

FTO, as an mA mRNA demethylase, is involved in various cancers. However, the role of FTO in clear cell renal cell carcinoma (ccRCC) remains unclear. In the present study, we discovered FTO is upregulated in ccRCC. Functionally, knockdown of FTO significantly impairs the proliferation and migration ability of ccRCC cells. Mechanistically, our data suggest FTO promotes the proliferation and migration of ccRCC through preventing degradation of PDK1 mRNA induced by YTHDF2 in an mA-dependent mechanism. Overall, our results identify the protumorigenic role of FTO through the mA/YTHDF2/PDK1 pathway, which could be a promising therapeutic target for ccRCC.