ArticleGenes & diseases2025
SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma.
Article in Genes & diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- PABPC1 in Cancer: From a Translational Housekeeper to a Stress-Responsive Regulatory Hub.Cancer science · 2026Review
- METTL16 promotes PD-L1 expression and mediates immunosuppression in B-cell lymphomas via mAmerican journal of translational research · 2026Article
- m6A-Targeted Cancer Therapy: Molecular Targets, Inhibitors, and Nanodelivery Strategies.International journal of nanomedicine · 2026Review
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solute carrier family 27 member 5 (SLC27A5/FATP5) is a liver-specific metabolic enzyme that plays a crucial role in fatty acid transport and bile acid metabolism. Deficiency of SLC27A5 promotes the progression of hepatocellular carcinoma (HCC) and is strongly associated with a poor prognosis. SLC27A5 exhibits noncanonical functions beyond its metabolic role; however, its specific mechanisms in hepatocarcinogenesis remain elusive and are therefore investigated in this study. Immunoprecipitation-mass spectrometry analysis showed that SLC27A5-interacting proteins were significantly enriched in alternative polyadenylation (APA). RNA-sequencing data provided evidence that SLC27A5 plays a global role in regulating APA events in HCC. Mechanistically, SLC27A5 facilitates the usage of the proximal polyadenylation site of
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Registered trials
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