ArticleNature communications2025
Mitochondrial-cytochrome c oxidase II promotes glutaminolysis to sustain tumor cell survival upon glucose deprivation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Integrated molecular mechanisms of salinity response in Apostichopus japonicus: focus on miRNA-driven core pathways and target gene regulation.Marine biotechnology (New York, N.Y.) · 2026Review
- The Redox Paradox of Natural Supplements in Cancer: A Narrative Review to Guide Clinical Practice.Antioxidants (Basel, Switzerland) · 2026Review
- Prolonged linezolid therapy induces progressive mitochondrial dysfunction in human peripheral blood mononuclear cells.Journal of translational medicine · 2026Article
- Nutrient stress-induced FTH1 safeguards redox balance and fuels pancreatic ductal adenocarcinoma growth while serving as a therapeutic target and diagnostic biomarker.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Review
- N-Acetylneuraminate Pyruvate Lyase Promotes Cell Adaptation to Glucose Deprivation by Regulating Intracellular ATP Levels.Current issues in molecular biology · 2026Article
- Brain Serotonin Deficiency Impairs Ovarian Reserve Function via the Hypothalamic-Pituitary-Ovarian Axis.Neuroscience bulletin · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Phosphoenolpyruvate carboxykinase 2 activation of the AMPK-CEBPB axis to enhance glutamine utilization to promote glycolysis and malignant behavior in adenocarcinomas cells under glucose deprivation.Journal of cell communication and signaling · 2026Article
- ΔNp63α drives serine synthesis to promote carboplatin resistance in NSCLC.Cell death & disease · 2026Article
- The molecular mechanism of IGF2BP3 promoting the malignant progression of lung cancer.Cancer cell international · 2026Review
- Unraveling the structure-activity relationship of alloying in nanozyme design for synergistic tumor metabolic-immunotherapy.Journal of nanobiotechnology · 2026Article
- An integrative omics-guided druggability analysis of VCX2 in hepatocellular carcinoma using Peruvian natural products.Frontiers in bioinformatics · 2026Article
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- Utilizing a novel mitochondrial-related gene signature for predicting the prognosis and immunological impact in bladder cancer.Discover oncology · 2025Article
- Phospholipid scramblases TMEM16F and Xkr8 mediate distinct features of phosphatidylserine (PS) externalization and immune suppression to promote tumor growth.Cell death discovery · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Dexmedetomidine preserves neuronal function by promoting mitochondrial biogenesis through the AMPK/PGC-1α pathway.In vitro cellular & developmental biology. Animal · 2025Article
- HADHA-mediated regulation of JAK/STAT3 signaling in glioblastoma: a metabolic-epigenetic axis.Cell death discovery · 2025Article
- Energy stress and adaptation strategy of tumor cells in different microenvironments: from primary tumors to distant metastases.Acta biochimica et biophysica Sinica · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Glucose deprivation, a hallmark of the tumor microenvironment, compels tumor cells to seek alternative energy sources for survival and growth. Here, we show that glucose deprivation upregulates the expression of mitochondrial-cytochrome c oxidase II (MT-CO2), a subunit essential for the respiratory chain complex IV, in facilitating glutaminolysis and sustaining tumor cell survival. Mechanistically, glucose deprivation activates Ras signaling to enhance MT-CO2 transcription and inhibits IGF2BP3, an RNA-binding protein, to stabilize MT-CO2 mRNA. Elevated MT-CO2 increases flavin adenosine dinucleotide (FAD) levels in activating lysine-specific demethylase 1 (LSD1) to epigenetically upregulate JUN transcription, consequently promoting glutaminase-1 (GLS1) and glutaminolysis for tumor cell survival. Furthermore, MT-CO2 is indispensable for oncogenic Ras-induced glutaminolysis and tumor growth, and elevated expression of MT-CO2 is associated with poor prognosis in lung cancer patients. Together, these findings reveal a role for MT-CO2 in adapting to metabolic stress and highlight MT-CO2 as a putative therapeutic target for Ras-driven cancers.
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