FTO promotes clear cell renal cell carcinoma progression via upregulation of PDK1 through an m(6)A dependent pathway

FTO, as an m(6)A 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 migratio...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374762/
https://www.ncbi.nlm.nih.gov/pubmed/35961973
http://dx.doi.org/10.1038/s41420-022-01151-w
Descripción
Sumario:FTO, as an m(6)A 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 m(6)A-dependent mechanism. Overall, our results identify the protumorigenic role of FTO through the m(6)A/YTHDF2/PDK1 pathway, which could be a promising therapeutic target for ccRCC.

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