ArticleCell death & disease2021
NDUFA4L2 promotes glioblastoma progression, is associated with poor survival, and can be effectively targeted by apatinib.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Targeting Metabolic Vulnerabilities in Glioblastoma: a Framework for Multi-node Combination Therapy.Current oncology reports · 2026Review
- Targeting TRIM25 as a therapeutic strategy to enhance ferroptosis in glioblastoma cells.Journal of nanobiotechnology · 2026Article
- Diagnostic and prognostic values of differentially expressed genes in canine mammary carcinoma: An integrated bioinformatics analysis.PloS one · 2026Article
- Tumor-Associated Pericytes: Tumorigenicity and Targeting for Cancer Therapy.Current vascular pharmacology · 2026Review
- Dynamic Metabolic States in TNBC: Orchestrating Spatiotemporal Adaptation and Therapy.Oncology research · 2026Review
- Mitochondrial electron transport chain gene-based prognostic model identifies SDHB as a key regulator of low-grade glioma progression and therapeutic target.Cancer cell international · 2025Article
- Towards the genome-scale discovery of bivariate monotonic classifiers.BMC bioinformatics · 2025Article
- Myeloid cell networks govern re-establishment of original immune landscapes in recurrent ovarian cancer.Cancer cell · 2025Article
- Identification of CAF signature genes and construction of CAF-based risk signature in hepatocellular carcinoma by multi-omics analysis.Frontiers in immunology · 2025Article
- Deciphering MARCH5's impact on multiple myeloma: insights into autophagy regulation and AKT-FOXO3 signaling.Blood neoplasia · 2024Article
- Single-cell RNA sequencing elucidated the landscape of breast cancer brain metastases and identified ILF2 as a potential therapeutic target.Cell proliferation · 2024Article
- Pancancer analysis of NDUFA4L2 with focused role in tumor progression and metastasis of colon adenocarcinoma.Medical oncology (Northwood, London, England) · 2024Article
- Exploring the metastasis-related biomarker and carcinogenic mechanism in liver cancer based on single cell technology.Heliyon · 2024Article
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- NDUFA4L2 reduces mitochondrial respiration resulting in defective lysosomal trafficking in clear cell renal cell carcinoma.Cancer biology & therapy · 2023Article
- Transcriptomic Analyses of Neurotoxic Astrocytes Derived from Adult Triple Transgenic Alzheimer's Disease Mice.Journal of molecular neuroscience : MN · 2023Article
- Transcriptional regulation of NDUFA4L2 by NFIB induces sorafenib resistance by decreasing reactive oxygen species in hepatocellular carcinoma.Cancer science · 2023Article
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- Human Tumor Targeted Cytotoxic Mast Cells for Cancer Immunotherapy.Frontiers in oncology · 2022Article
Corrections and comments
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10 authors.
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Abstract
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex, 4-like 2 (NDUFA4L2) is a subunit of Complex I of the mitochondrial respiratory chain, which is important in metabolic reprogramming and oxidative stress in multiple cancers. However, the biological role and molecular regulation of NDUFA4L2 in glioblastoma (GBM) are poorly understood. Here, we found that NDUFA4L2 was significantly upregulated in GBM; the elevated levels were correlated with reduced patient survival. Gene knockdown of NDUFA4L2 inhibited tumor cell proliferation and enhanced apoptosis, while tumor cells initiated protective mitophagy in vitro and in vivo. We used lentivirus to reduce expression levels of NDUFA4L2 protein in GBM cells exposed to mitophagy blockers, which led to a significant enhancement of tumor cell apoptosis in vitro and inhibited the development of xenografted tumors in vivo. In contrast to other tumor types, NDUFA4L2 expression in GBM may not be directly regulated by hypoxia-inducible factor (HIF)-1α, because HIF-1α inhibitors failed to inhibit NDUFA4L2 in GBM. Apatinib was able to effectively target NDUFA4L2 in GBM, presenting an alternative to the use of lentiviruses, which currently cannot be used in humans. Taken together, our data suggest the use of NDUFA4L2 as a potential therapeutic target in GBM and demonstrate a practical treatment approach.
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