ArticleJournal of translational medicine2025
Endogenous protein S100A14 stabilizes glutaminase to render hepatocellular carcinoma resistant to sorafenib.
Article in Journal of translational medicine, 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.
- Real-time NMR analysis of glutamine metabolism for screening anti-cancer agents in living cells.Magnetic resonance letters · 2027Article
- Host-directed antiviral strategy targeting prohibitins: Mel56 suppresses influenza A virus and severe acute respiratory syndrome coronavirus 2 via modulation of antioxidant pathways and mitochondrial function.Microbiology spectrum · 2026Article
- Cabozantinib activates TFEB-mediated autophagy to exert anti-tumor effects in hepatocellular carcinoma.In vitro cellular & developmental biology. Animal · 2026Article
- Post-translational modification in hepatocellular carcinoma resistance: molecular mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundMany cases of advanced hepatocellular carcinoma (HCC) are resistant to the widely used drug sorafenib, which worsens prognosis. While many studies have explored how acquired resistance emerges during drug exposure, the mechanism underlying primary resistance before treatment still remain elusive.
methodsSingle-cell lineage tracing and RNA sequencing were performed to identify primary sorafenib-resistant lineages in HCC. Differential gene expression analysis was employed to identify the biomarkers of drug-resistant lineage cells. Cell viability and colony formation assays were adopted to assess the involvement of S100A14 on sorafenib resistance. Co-immunoprecipitation (CO-IP) and mass spectrometry analysis were conducted to uncover the downstream targets and regulatory mechanisms of S100A14 in primary resistance to sorafenib. In vivo mouse xenograft experiments were carried out to assess the effect of S100A14 or its interacting protein glutaminase (GLS) on primary resistance to sorafenib in HCC.
resultsSingle-cell lineage tracing identified a cluster of sorafenib primary resistant cells, and S100A14, a Ca
conclusionsOur results demonstrate that S100A14 plays a pivotal role in promoting primary resistance to sorafenib by stabilizing GLS to reduce oxidative stress, and acts as a potential therapeutic target to enhance the efficacy of sorafenib in HCC patients.
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