YTHDF1 upregulation mediates hypoxia-dependent breast cancer growth and metastasis through regulating PKM2 to affect glycolysis.

ABSTRACT: N6-methyladenosine modification is the most common RNA modification mechanism in mammals. YTHDF1, a m⁶A reader, can recognize the m⁶A of mRNAs to facilitate the interaction with the mRNA ribosome assembly and recruitment of translation initiators to promote translation. From a clinical perspective, YTHDF1 upregulation is frequently observed in breast cancer, but its involvement in those cancer-related events is still unclear. Here we report that YTHDF1 is a cancer driver capable of facilitating the proliferation and invasion of breast cancer cells as well as enhancing tumorigenicity and metastasis through promoting glycolysis. We found that tumor hypoxia can transcriptionally induce HIF1α and post-transcriptionally inhibit the expression of miR-16-5p to promote YTHDF1

SUBMITTER: Yao X 

PROVIDER: S-EPMC8940925 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature