ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021
A Nuclear Long Non-Coding RNA LINC00618 Accelerates Ferroptosis in a Manner Dependent upon Apoptosis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers.
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Who cites it
178 citing papers in PubMed, 287 citations in OpenAlex.
- Risk stratification of lung adenocarcinoma using a nomogram combined with ferroptosis-related LncRNAs and subgroup analysis with immune and N6-methyladenosine modification.BMC medical genomics · 2022Trial
- Mouse Bone Mesenchymal Stem Cells Attenuate Apoptosis by Regulating the Bcl2/Caspase3 Signaling Pathway in Premature Ovarian Failure.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Review
- CTSZ-dependent anoikis resistance enhances malignant characters of glioblastoma via NF-κB signaling.iScience · 2026Article
- Article
- Liquid-liquid phase separation-driven regulated cell death: from molecular mechanisms to therapeutic strategies.Cell death discovery · 2026Review
- Non-coding RNAs as master regulators of ferroptosis in cancer: mechanisms and clinical implications.Molecular cancer · 2026Review
- Abnormal iron homeostasis mediates cochlear hair cell impairment and hearing loss in Gprasp2-deficient mice.Communications biology · 2026Article
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- Macrophage ferroptosis in hematologic malignancies: emerging mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Mechanistic Approach to Ferroptosis in Cancer and Neurological Diseases.Current drug targets · 2026Review
- NAMPT inhibition induces ferroptosis via mitochondrial metabolic reprogramming to enhance tumour immunogenicity in glioblastoma.Frontiers in immunology · 2026Article
- Ferroptosis in hematological malignancies: molecular mechanisms and therapeutic potential.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Ferroptosis-Mediated Cell-Specific Damage: Molecular Cascades and Therapeutic Breakthroughs in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2025Review
- Unveiling the metal-driven death: ferroptosis and cuproptosis in leukemia.European journal of medical research · 2025Review
- Genome-wide cross-trait analysis of heterogeneous outcomes in early life atopic dermatitis.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025Article
- Ferroptosis rewired: ncRNA gatekeepers as pharmacological targets in hepatocellular carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Non-coding RNAs-regulated SLC7A11 modulates ferroptosis: a new strategy for cancer therapy.Functional & integrative genomics · 2025Review
- Influenza a(H1N1) virus infection impairs syncytiotrophoblast functions by promoting ferroptosis through the TNF-α/ISG15/EGR1 axis.Virology journal · 2025Article
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
118 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is primarily caused by intracellular iron catalytic activity and lipid peroxidation. The potential interplay between ferroptosis and apoptosis remains poorly understood. Here, we show that the expression of a nuclear long non-coding RNA (lncRNA), LINC00618, is reduced in human leukemia and strongly increased by vincristine (VCR) treatment. Furthermore, LINC00618 promotes apoptosis by increasing the levels of BCL2-Associated X (BAX) and cleavage of caspase-3. LINC00618 also accelerates ferroptosis by increasing the levels of lipid reactive oxygen species (ROS) and iron, two surrogate markers of ferroptosis, and decreasing the expression of solute carrier family 7 member 11 (SLC7A11). Interestingly, VCR-induced ferroptosis and apoptosis are promoted by LINC00618, and LINC00618 accelerates ferroptosis in a manner dependent upon apoptosis. LINC00618 attenuates the expression of lymphoid-specific helicase (LSH), and LSH enhances the transcription of SLC7A11 after the recruitment to the promoter regions of SLC7A11, further inhibiting ferroptosis. Knowledge of these mechanisms demonstrates that lncRNAs related to ferroptosis and apoptosis are critical to leukemogenesis and chemotherapy.
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