ArticleTranslational cancer research2025
Inhibition of SLC25A10 promotes cellular senescence and impedes hepatocellular carcinoma progression.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- MechAInistic: A Reviewer-Supervised Multi-Agent LLM System for Auditable Mechanistic Drug-Hypothesis Generation.bioRxiv : the preprint server for biology · 2026Article
- A senescence-based machine learning model prognosticates and personalizes therapy in cervical cancer.Translational cancer research · 2026Article
- Nuclear translocation of SLC25A10 isoform 3 promotes chemoresistance in HCC cells via CEBPB/BCL2A1 signaling.Cell death & disease · 2026Article
- Comprehensive Evaluation and Validation Reveal Mitochondrial Solute Carrier SLC25A3 as a Novel Prognostic Biomarker and Therapeutic Target in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
- SLC25A3 promotes hepatocellular carcinoma progression by inducing mitochondrial dysfunction and chromatin remodeling.Translational cancer research · 2025Article
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Authors and funding
9 authors.
Funding
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Abstract
Background: Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality with limited therapeutic options. Solute carrier family 25 member 10 (SLC25A10), a mitochondrial transporter linked to metabolic regulation and tumor progression, has unclear roles in HCC pathogenesis. This study aimed to elucidate the functional and mechanistic contributions of SLC25A10 to HCC development. Methods: The International Cancer Genome Consortium (ICGC) database, GAO Results: The protein and messenger RNA (mRNA) levels of SLC25A10 in HCC tissues were higher than those in adjacent normal tissues. Knockdown of SLC25A10 suppressed cell proliferation, induced senescence-associated β-galactosidase activity, and triggered G1 phase arrest by downregulating cyclin-dependent kinase 4 ( Conclusions: SLC25A10 promotes HCC progression by suppressing cellular senescence. Pharmacological or genetic inhibition of SLC25A10 triggers tumor suppression through HMGB1-mediated SASP signaling, positioning SLC25A10 as a promising therapeutic target for HCC intervention.
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