ArticleActa pharmacologica Sinica2022
Apolipoprotein C1 promotes glioblastoma tumorigenesis by reducing KEAP1/NRF2 and CBS-regulated ferroptosis.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- Significance of GSH and HRedox report : communications in free radical research · 2026Review
- GD3s-mediated lipid metabolism reprograming promotes proliferation and metastasis of melanoma.Journal of translational medicine · 2026Article
- Ferroptosis in Glioblastoma and Neuroblastoma: Molecular Mechanisms and Novel Therapeutic Strategies.Current issues in molecular biology · 2026Review
- LAR1 promotes breast carcinogenesis by activating NF-κB signaling pathway through binding and enhancing APOC1 expression.iScience · 2026Article
- Unlocking glioma vulnerabilities: targeting regulated cell death pathways for innovative therapies.Cell death discovery · 2026Review
- Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis.Chinese medicine · 2026Article
- Ferroptosis and metabolic reprogramming in the immunosuppressive microenvironment of glioblastoma: emerging mechanisms and novel strategies.Frontiers in immunology · 2026Review
- Dynamic release of extracellular particles after opening of the blood-brain barrier predicts glioblastoma susceptibility to paclitaxel.Nature communications · 2025Article
- Oxidative Stress and Iron Addiction: A Comparative Study of 1321N1 Astrocytoma and T98G Glioblastoma Cells with Differential Expression of L-Cysteine-Metabolizing Enzymes.Biomolecules · 2025Article
- Review
- Collagen type I alpha 1 induces radio-resistance in hypoxic glioblastoma cells by promoting autophagy.Journal of neuro-oncology · 2025Article
- KIAA1429 Silencing ameliorates osteosarcoma progression through promoting ferroptosis via Nrf2/NQO1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- EPAS1 amplifies asthma pathogenesis through JAK2/STAT3-mediated ferroptosis and inflammation.Biomolecules & biomedicine · 2025Article
- Review
- Article
- Mapping glioma progression: single-cell RNA sequencing illuminates cell-cell interactions and immune response variability.Discover oncology · 2025Article
- Ferroptosis Transcriptional Regulation and Prognostic Impact in Medulloblastoma Subtypes Revealed by RNA-Seq.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial Regulation of Ferroptosis in Cancer Cells.International journal of biological sciences · 2025Review
- Procyanidin B1 Promotes PSMC3-NRF2 Ubiquitination to Induce Ferroptosis in Glioblastoma.Phytotherapy research : PTR · 2024Article
- Ferroptosis: Potential therapeutic targets and prognostic predictions for acute myeloid leukemia (Review).Oncology letters · 2024Review
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM), a malignant brain tumor, is a world-wide health problem because of its poor prognosis and high rates of recurrence and mortality. Apolipoprotein C1 (APOC1) is the smallest of apolipoproteins, implicated in many diseases. Recent studies have shown that APOC1 promotes tumorigenesis and development of several types of cancer. In this study we investigated the role of APOC1 in GBM tumorigenesis. Using in silico assays we showed that APOC1 was highly expressed in GBM tissues and its expression was closely related to GBM progression. We showed that APOC1 protein expression was markedly increased in four GBM cell lines (U251, U138, A172 and U87) compared to the normal brain glia cell lines (HEB, HA1800). In U251 cells, overexpression of APOC1 promoted cell proliferation, migration, invasion and colony information, which was reversed by APOC1 knockdown. APOC1 knockdown also markedly inhibited the growth of GBM xenografts in the ventricle of nude mice. We further demonstrated that APOC1 reduced ferroptosis by inhibiting KEAP1, promoting nuclear translocation of NRF2 and increasing expression of HO-1 and NQO1 in GBM cells. APOC1 also induced ferroptosis resistance by increasing cystathionine beta-synthase (CBS) expression, which promoted trans-sulfuration and increased GSH synthesis, ultimately leading to an increase in glutathione peroxidase-4 (GPX4). Thus, APOC1 plays a key role in GBM tumorigenesis, conferring resistance to ferroptosis, and may be a promising therapeutic target for GBM.
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