SPI1-induced downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner.

ABSTRACT: As one of the most common post-transcriptional modifications of mRNAs and noncoding RNAs, N⁶-methyladenosine (m⁶A) modification regulates almost every aspect of RNA metabolism. Evidence indicates that dysregulation of m⁶A modification and associated proteins contributes to glioblastoma (GBM) progression. However, the function of fat mass and obesity-associated protein (FTO), an m⁶A demethylase, has not been systematically and comprehensively explored in GBM. Here, we found that decreased FTO expression in clinical specimens correlated with higher glioma grades and poorer clinical outcomes. Functionally, FTO inhibited growth and invasion in GBM cells in vitro and in vivo. Mechanistically, FTO regulated the m⁶A modification

SUBMITTER: Zhang S 

PROVIDER: S-EPMC8905236 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature