ArticleAmerican journal of cancer research2023
LINC02362/hsa-miR-18a-5p/FDX1 axis suppresses proliferation and drives cuproptosis and oxaliplatin sensitivity of hepatocellular carcinoma.
Article in American journal of cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 28 citations in OpenAlex.
- LncRNA GAS5 Restrains Hepatocellular Carcinoma by Targeting the miR-18a-5p-CADM2 Axis.Biochemical genetics · 2026Article
- Harnessing copper-iron crosstalk: A novel strategy to combat hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- 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
- Research Progress on Elesclomol-Induced Cuproptosis for Antitumor Effects.Biomedicines · 2026Review
- Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026Review
- Targeting copper death-related long non-coding RNAs: a novel strategy to overcome immunotherapy resistance in liver cancer.Frontiers in immunology · 2026Review
- Comparative analysis of lncRNA-mRNA networks in albendazole-resistant Haemonchus contortus.Genes & genomics · 2026Article
- DACT1 inhibits cuproptosis and promotes cell malignancy via activation of PI3K/AKT signaling in laryngeal squamous cell carcinoma.European journal of medical research · 2025Article
- Icaritin suppresses CAD-mediated liver cancer development by targeting miR-18b-5p in a xenograft mouse model.Medical oncology (Northwood, London, England) · 2025Article
- Copper Homeostasis and Cuproptosis As Potential Intervention Strategy in Atherosclerosis.Journal of cardiovascular translational research · 2025Review
- Epigenetic modification of cuproptosis by non-coding RNAs in cancer drug resistance.Molecular cancer · 2025Review
- Liver-specific lncRNAs associated with liver cancers.FEBS open bio · 2025Review
- Cuproptosis and Cardiovascular Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies-A Narrative Review.Reviews in cardiovascular medicine · 2025Review
- Article
- Immune infiltration related PRDX4 facilitates the malignant features and drug resistance of breast cancer.Scientific reports · 2025Article
- Increased CDKN2A expression correlates with resistance to platinum-based therapy and decreased infiltration of B lymphocytes in colon adenocarcinoma.Functional & integrative genomics · 2025Article
- The Pleiotropic Role of the MicroRNA-17-92 Cluster in Cardiovascular Diseases and Cancer.Reviews in cardiovascular medicine · 2025Review
- Taxifolin regulates SLC31A1-mediated cuproptosis and tumor progression in hepatocellular carcinoma.Human cell · 2025Article
- Cuproptosis related lncRNA signature as a prognostic and therapeutic biomarker in osteosarcoma immunity.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis is a novel cell death mechanism caused by copper overload, with FDX1 serving as the key regulator. LncRNAs are known to play a significant role in the aberrant regulation of gene expression in hepatocellular carcinoma (HCC). In this study, we investigated the biological role of the LINC02362/hsa-miR-18a-5p/FDX1 axis in HCC. We first explored the expression pattern, prognostic value, biological functions, drug sensitivity, and immune effect of FDX1. Using bioinformatics techniques, we then predicted several potential target lncRNAs and miRNAs. We identified a lncRNA-miRNA-FDX1 axis based on the ceRNA mechanism. In vitro experiments were conducted to validate the relationship between the lncRNA-miRNA-FDX1 axis and its biological effects in HCC. Finally, we investigated the relationship between the LINC02362/hsa-miR-18a-5p/FDX1 axis and oxaliplatin-induced cuproptosis in HCC. Our findings indicated that FDX1 expression was downregulated in HCC tissues; however, elevated FDX1 expression correlates with improved prognosis and heightened sensitivity to oxaliplatin. We confirmed that LINC02362 binds to and directly regulates the expression of miR-18a-5p, with FDX1 a target of miR-18a-5p. Experimental results suggested that upregulating LINC02362/hsa-miR-18a-5p/FDX1 axis suppressed the proliferation of HCC cells. Furthermore, LINC02362 knockdown led to a reduction in copper concentration and resistance to elesclomol-Cu. We also discovered that augmenting the LINC02362/hsa-miR-18a-5p/FDX1 axis could bolster the sensitivity of HCC to oxaliplatin through cuproptosis. This work presents the LINC02362/hsa-miR-18a-5p/FDX1 axis as a novel pathway that triggers cuproptosis and enhances the sensitivity of HCC to oxaliplatin, presenting a promising therapeutic avenue to combat oxaliplatin resistance in HCC.
Indexed as
Identifiers
38058825PMC10695789W4389452407What OpenQuestion holds
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.