ArticleSmart medicine2025
Targeting KRAS Sensitizes Ferroptosis by Coordinately Regulating the TCA Cycle and Nrf2-SLC7A11-GPX4 Signaling in Hepatocellular Carcinoma.
Article in Smart medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Super-enhancer-driven KIAA1522 upregulation suppresses ferroptosis in hepatocellular carcinoma.Clinical and translational medicine · 2026Article
- Research Progress on Elesclomol-Induced Cuproptosis for Antitumor Effects.Biomedicines · 2026Review
- Apolipoprotein C3 exacerbates vascular calcification by promoting ferroptosis via the TLR2/AMPK pathway in vascular smooth muscle cells.Redox biology · 2026Article
- Phillygenin suppresses hepatocellular carcinoma progression by modulating the TNF signaling pathway and TCA cycle metabolism.Frontiers in pharmacology · 2026Article
- Ferrocene-Modified Nanoscale Covalent Organic Frameworks for Ferroptosis-Based Sonodynamic Therapy Inhibit Breast Cancer and Its Bone Metastasis.Cyborg and bionic systems (Washington, D.C.) · 2026Article
- [Gastrodin inhibits ferroptosis to alleviate hypoxic-ischemic brain damage in neonatal mice by activating GPX4/SLC7A11/FTH1 signaling].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- A lactylation-ferroptosis cross-talk gene signature predicts hepatocellular carcinoma prognosis and reveals STMN1/PRDX1 as therapeutic targets.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenic KRAS, a notorious driver of cancer progression, remains a therapeutic challenge. In hepatocellular carcinoma (HCC), KRAS overexpression correlates with tumor aggressiveness. Here, we demonstrate that NSC48160 induces HCC cell death by suppressing KRAS expression. Metabolomic profiling revealed that NSC48160 significantly enhances intracellular tricarboxylic acid (TCA) cycle activity and fructose metabolism, disrupting redox homeostasis, and triggering ferroptosis. Combining NSC48160 with the SLC7A11 inhibitor HG106 synergistically eliminated HCC cells in vitro and suppressed tumor growth in vivo. Mechanistically, NSC48160 indirectly inhibits the Nrf2-SLC7A11-GPX4 axis, as evidenced by ferroptosis-pathway array assays. Specifically, NSC48160 downregulates Nrf2 expression, thereby suppressing its downstream targets GPX4 and SLC7A11, ultimately promoting ferroptosis. Our findings establish NSC48160 as a novel KRAS inhibitor that induces ferroptosis through metabolic and redox reprogramming, offering a promising therapeutic strategy for KRAS-driven HCC.
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