ArticleCell death discovery2025
C12ORF49 inhibits ferroptosis in hepatocellular carcinoma cells via reprogramming SREBP1/SCD1-mediated lipid metabolism.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- The pivotal role of SCD1 in digestive cancers: Bridging lipid metabolic reprogramming and programmed cell death (Review).International journal of oncology · 2026Review
- Review
- [Mechanism ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Stearoyl-CoA desaturase 1 integrates tissue-specific oncogenic pathways into a pan-cancer ferroptosis resistance program.Cell death & disease · 2026Review
- FTO-Catalysed Demethylation of LUR1 mRNA Suppresses Macrophage Lipid Accumulation and Aortic Atherosclerosis.Journal of cellular and molecular medicine · 2026Article
- Combinatorial treatment with donafenib and quercetin suppresses lipid metabolism in HepG2 cells by targeting the CREB1/DRP1/SREBP1 axis.Translational cancer research · 2026Article
- SREBP1 knockdown triggers ferroptosis by suppressing the Nrf2-XCT/GPX4 axis in ovarian cancer.Cell death discovery · 2026Article
- Targeting C12ORF49-Mediated Ferroptosis in Hepatocellular Carcinoma.JGH open : an open access journal of gastroenterology and hepatology · 2026Review
- Article
- Machine learning-powered discovery of a novel berberine derivative inducing SCD-dependent ferroptosis in osteosarcoma.Journal of translational medicine · 2025Article
- SPRINGing off the lock: the role of SPRING in S1P activity and SREBP-regulated lipid metabolism.Current opinion in lipidology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
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, C12ORF49 promotes SREBP1/SCD-regulated production of monounsaturated fatty acids, which inhibits ferroptosis in HCC cells. Furthermore, silencing C12ORF49 combined with Sorafenib treatment showed a synergistic effect in inducing HCC cell death. Together, our findings suggest a critical role of C12ORF49 in the evasion of ferroptosis in HCC cells, highlighting the potential of targeting C12ORF49 as a therapeutic strategy to enhance the efficacy of Sorafenib treatment in HCC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.