C12ORF49 inhibits ferroptosis in hepatocellular carcinoma cells via reprogramming SREBP1/SCD1-mediated lipid metabolism.

ABSTRACT: Altered lipid metabolism is an emerging hallmark of cancer, which is involved in various aspects of the cancer phenotypes. C12ORF49 has recently been identified as a pivotal regulator of sterol regulatory element binding proteins (SREBPs), a family of transcriptional factors that govern lipid biosynthesis. Nevertheless, the function of C12ORF49 in human cancers has not been studied. Here, we show that C12ORF49 levels are higher in HCC tissue than in nearby non-cancerous liver tissue. Additionally, increased C12ORF49 expression is linked to poorer survival outcomes in HCC patients. Functional experiments uncovered that knockdown of C12ORF49 inhibited HCC cell survival and tumor growth by inducing ferroptosis, whereas the opposites were observed upon C12ORF49 overexpression. Mechanistically,

SUBMITTER: Yu HC 

PROVIDER: S-EPMC12003882 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature