FMRP protects breast cancer cells from ferroptosis by promoting SLC7A11 alternative splicing through interacting with hnRNPM.

ABSTRACT: Ferroptosis is a unique modality of regulated cell death that is driven by iron-dependent phospholipid peroxidation. N6-methyladenosine (m⁶A) RNA modification participates in varieties of cellular processes. However, it remains elusive whether m⁶A reader Fragile X Mental Retardation Protein (FMRP) are involved in the modulation of ferroptosis in breast cancer (BC). In this study, we found that FMRP expression was elevated and associated with poor prognosis and pathological stage in BC patients. Overexpression of FMRP induced ferroptosis resistance and exerted oncogenic roles by positively regulating a critical ferroptosis defense gene SLC7A11. Mechanistically, upregulated FMRP catalyzes m⁶A modification of SLC7A11 mRNA and further influences the SLC7A11 tra

SUBMITTER: Wang N 

PROVIDER: S-EPMC11497378 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature