ArticleCommunications biology2025
Copper-mediated SEC14L3 promotes cuproptosis to inhibit hepatocellular carcinoma growth via ERK/YY1/FDX1 axis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- GSH-responsive self-assembled nanoplatform synergistically enhances cuproptosis through metabolic reprogramming and oxidative stress amplification.Materials today. Bio · 2026Article
- Harnessing copper-iron crosstalk: A novel strategy to combat hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026Review
- ATP7A Orchestrates Tumor Progression and Cuproptosis in Hepatocellular Carcinoma via the LINC02038-miR-506-3p Regulatory Circuit.Journal of biochemical and molecular toxicology · 2026Article
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026Review
- Cuproptosis: potential new direction in liver-related diseases research and treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- XN@CuO/HA nanobipyramids trigger FOXO1-GADD45G-mediated cuproptosis and synergy with anti-PD-1 for lung cancer therapy.Materials today. Bio · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Copper modulates cell fate through the PLK1-FOXO3a-β-catenin signaling pathway by differentially regulating cuproptosis and EMT.Apoptosis : an international journal on programmed cell death · 2026Article
- Cuproptosis-Related genes as potential core targets for the Diagnosis, Therapy, and prognosis of glioblastoma.Functional & integrative genomics · 2026Article
- Roles of cuproptosis in central nervous system tumors: from molecular mechanisms to therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
- Development of a recurrence-related gene signature and functional role of MLLT6 in ovarian cancer progression and Paclitaxel resistance.Journal of ovarian research · 2025Article
- Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders.Cell death discovery · 2025Review
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- Mechanisms of copper metabolism and cuproptosis: implications for liver diseases.Frontiers in immunology · 2025Review
- Copper metabolism and cuproptosis: broad perspectives in the treatment of hepatocellular carcinoma.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis, a copper-triggered cell death pathway, holds therapeutic potential for cancers, but its regulatory mechanisms in hepatocellular carcinoma (HCC) remain undefined. Despite SEC14L3's known roles in cellular signaling, its involvement in HCC progression and cuproptosis regulation is unclear. Here, we reveal that SEC14L3 expression is downregulated in HCC cells and tissues and correlates with advanced stages and poor prognosis. Copper-induced cuproptosis inhibits HCC cell viability, and SEC14L3 positively modulates cuproptosis in HCC cells by promoting DLAT lipoylation and its oligomerization. Mechanistically, SEC14L3-mediated cuproptosis suppressed HCC growth via the ERK/YY1/FDX1 axis both in vitro and in vivo. Additionally, copper enhanced the SEC14L3 expression, which in turn regulated ERK/YY1/FDX1 axis. Our findings show that copper-mediated SEC14L3 promotes cuproptosis via ERK/YY1/FDX1 axis, thereby inhibiting HCC growth. These insights provide a mechanistic foundation for targeting cuproptosis, advancing the development of SEC14L3-driven therapeutic strategies for HCC.
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