ArticleCancer research2019
Mitochondrial NIX Promotes Tumor Survival in the Hypoxic Niche of Glioblastoma.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed, 88 citations in OpenAlex.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Kaempferide in Alpinia officinarum Hance Exerts Anti-Hepatocellular Carcinoma Activity by Inhibiting Mitophagy Through Downregulation of BNIP3L.Journal of cellular and molecular medicine · 2026Article
- Molecular diversity of mitochondrial autophagy receptors: context-dependent effects in human health and disease.Cell death discovery · 2026Review
- Article
- Mitochondrial ribosomal protein MRPL27 supports glioma malignancy through regulation of oxidative phosphorylation.Cellular and molecular life sciences : CMLS · 2026Article
- DNA methylation-mediated regulation of hypoxia-responsive genes facilitates high-altitude adaptation in Tibetan chickens.Poultry science · 2026Article
- A Review of HIF-1α-Mediated Integration of Metabolic Reprogramming, Mitochondrial Function, and PI3K/Akt-MAPK-Nrf2-NF-κB Signaling.Antioxidants (Basel, Switzerland) · 2026Review
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
- Decoding myeloid heterogeneity in glioblastoma: spatial insights from transcriptomics.Journal of translational medicine · 2026Review
- Dual Roles of NIX/BNIP3L in Tumors: Friend or Foe.Biology · 2026Review
- Reprogramming neural-tumor crosstalk: emerging therapeutic dimensions and targeting strategies.Military Medical Research · 2025Review
- BNIP3L/BNIP3-Mediated Mitophagy Contributes to the Maintenance of Ovarian Cancer Stem Cells.Journal of cellular and molecular medicine · 2025Article
- Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Neuropeptide Signaling in Glioblastoma: A Comprehensive Review of the Current State and Future Direction.Neuromolecular medicine · 2025Review
- The promise of mitochondria in the treatment of glioblastoma: a brief review.Discover oncology · 2025Review
- Interactions between ferroptosis and tumour development mechanisms: Implications for gynaecological cancer therapy (Review).Oncology reports · 2025Review
- Role of Hypoxia-Associated Long Noncoding RNAs in Cancer Chemo-Therapy Resistance.International journal of molecular sciences · 2025Review
- Deapioplatycodin D inhibits glioblastoma cell proliferation by inducing BNIP3L-mediated incomplete mitophagy.Cancer cell international · 2025Article
- Mitophagy in the mechanisms of treatment resistance in solid tumors.Oncology reviews · 2025Review
- Expression and Clinical Significance of BCL2 Interacting Protein 3 Like (BNIP3L) in Serum of Patients with MM.Blood and lymphatic cancer : targets and therapy · 2025Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Cancer cells rely on mitochondrial functions to regulate key survival and death signals. How cancer cells regulate mitochondrial autophagy (mitophagy) in the tumor microenvironment as well as utilize mitophagy as a survival signal is still not well understood. Here, we elucidate a key survival mechanism of mitochondrial NIX-mediated mitophagy within the hypoxic region of glioblastoma, the most malignant brain tumor. NIX was overexpressed in the pseudopalisading cells that envelop the hypoxic-necrotic regions, and mitochondrial NIX expression was robust in patient-derived glioblastoma tumor tissues and glioblastoma stem cells. NIX was required for hypoxia and oxidative stress-induced mitophagy through NFE2L2/NRF2 transactivation. Silencing NIX impaired mitochondrial reactive oxygen species clearance, cancer stem cell maintenance, and HIF/mTOR/RHEB signaling pathways under hypoxia, resulting in suppression of glioblastoma survival
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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.