ArticleFrontiers in oncology2022
Silenced LINC01134 Enhances Oxaliplatin Sensitivity by Facilitating Ferroptosis Through GPX4 in Hepatocarcinoma.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Sanguinarine chloride inducing ferroptosis and downregulating GPX4 expression in liver cancer: An integratedExperimental and therapeutic medicine · 2026Article
- Non-coding RNAs as master regulators of ferroptosis in cancer: mechanisms and clinical implications.Molecular cancer · 2026Review
- Artificial intelligence applications in oxaliplatin-based chemotherapy for colon cancer: advancing prognosis, toxicity prediction, and dose personalization.Frontiers in pharmacology · 2026Review
- Extrachromosomal microDNA Signature as a Candidate Biomarker in Pediatric Acute Lymphoblastic Leukemia.Cancer research communications · 2026Article
- Exploring Long Noncoding RNAs as Regulators of Tumor Ferroptosis: Advances and Challenges.Cancer science · 2025Review
- Identification and validation of a ferroptosis-related long non-coding RNA signature as a prognostic biomarker for hepatocellular carcinoma.Journal of gastrointestinal oncology · 2025Article
- Targeting ferroptosis: the role of non-coding RNAs in hepatocellular carcinoma progression and therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Deciphering the mechanisms of long non-coding RNAs in ferroptosis: insights into its clinical significance in cancer progression and immunology.Cell death discovery · 2025Review
- Role of long non-coding RNAs in the regulation of ferroptosis in tumors.Frontiers in immunology · 2025Review
- Non-coding RNA: A key regulator in the Glutathione-GPX4 pathway of ferroptosis.Non-coding RNA research · 2024Review
- Ferroptosis: a new promising target for hepatocellular carcinoma therapy.Molecular and cellular biochemistry · 2024Review
- Ferroptosis-related oxaliplatin resistance in multiple cancers: Potential roles and therapeutic Implications.Heliyon · 2024Review
- Regulating ferroptosis by non-coding RNAs in hepatocellular carcinoma.Biology direct · 2024Review
- Epigenetic modification of ferroptosis by non-coding RNAs in cancer drug resistance.Molecular cancer · 2024Review
- SNHG4-mediated PTEN destabilization confers oxaliplatin resistance in colorectal cancer cells by inhibiting ferroptosis.Apoptosis : an international journal on programmed cell death · 2024Article
- Ferroptotic therapy in cancer: benefits, side effects, and risks.Molecular cancer · 2024Review
- Long non-coding RNAs in ferroptosis, pyroptosis and necroptosis: from functions to clinical implications in cancer therapy.Frontiers in oncology · 2024Review
- Breaking the Barriers of Therapy Resistance: Harnessing Ferroptosis for Effective Hepatocellular Carcinoma Therapy.Journal of hepatocellular carcinoma · 2024Review
- Current Progress of Ferroptosis Study in Hepatocellular Carcinoma.International journal of biological sciences · 2024Review
- Review
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Authors and funding
12 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Recently, long noncoding RNA LINC01134 has been shown to reduce cell viability and apoptosis Methods: Bioinformatics analysis was employed to screen lncRNAs positively correlated with GPX4 and poor clinical prognosis. And Western blot and RT-PCR analysis in HCC cells confirmed the effect of LINC01134 on GPX4 expression. In addition, LINC01134 siRNA was transfected in HCC cells to detect the changes in cell viability, ROS, lipid peroxidation, MDA levels and GSH/GSSG levels. CCK-8, colony formation and apoptosis assays were performed to determine the effect of LINC01134 on cell death. The effect of LINC01134 and OXA on Nrf2 transcriptional binding to GPX4 was analyzed using dual luciferase reporter assay and CHIP. The expression of GPX4 and Nrf2 in HCC tissues was detected by FISH and IHC. Results: LINC01134 is a novel lncRNA positively correlated with GPx4 and associated with poor clinical prognosis. Silenced LINC01134 conferred OXA sensitivity by enhancing total ROS, lipid ROS, MDA levels and decreasing GSH/GSSG ratio. Mechanistically, LINC01134 and OXA could promote Nrf2 recruitment to the GPX4 promoter region to exert transcriptional regulation of GPX4. Clinically, LINC01134 was positively correlated with GPX4 or Nrf2, demonstrating the clinical significance of LINC01134, Nrf2 and GPX4 in OXA resistance of HCC. Conclusions: We identified LINC01134/Nrf2/GPX4 as a novel and critical axis to regulate HCC growth and progression. Targeting GPX4, knocking down LINC01134 or Nrf2 could be a potential therapeutic strategy for HCC.
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