ArticlePloS one2015
Down-Regulation of NDUFB9 Promotes Breast Cancer Cell Proliferation, Metastasis by Mediating Mitochondrial Metabolism.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- Article
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- Complex I protein NDUFB9 is a metabolic vulnerability in triple negative breast cancer brain metastases.Nature communications · 2026Article
- Identification and verification of hub genes related to mitochondrial dysfunction in epilepsy based on bioinformatics analysis.BMC neurology · 2026Article
- The role of LLPS of biomacromolecules in the gonads and related diseases.Frontiers in endocrinology · 2026Review
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Roles of mitochondrial complexes in non-alcoholic fatty liver disease.Frontiers in molecular biosciences · 2026Review
- Obesity-Associated TRIM15 Promotes the Proliferation of Esophageal Adenocarcinoma Through the YY2/FOXRED1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cytochrome c oxidase dependent respiration is essential for T cell activation, proliferation and memory formation.Nature communications · 2025Article
- Mitochondrial Dysfunction in Apoptosis-Resistant Acute Myeloid Leukemia Cells During a Sterile Inflammatory Response.Biomolecules · 2025Article
- NDUFB9 ameliorates CUMS-induced depression-like behavior by promoting mitophagy.Translational psychiatry · 2025Article
- Rotenone adaptation promotes migration and invasion of p53-wild-type colon cancer through lipid metabolism.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Single-Cell RNA and Transcriptome Sequencing to Analyze the Role of Lactate Metabolism in Traumatic Brain Injury Astrocytes.Brain and behavior · 2025Article
- Copy number amplification of FLAD1 promotes the progression of triple-negative breast cancer through lipid metabolism.Nature communications · 2025Article
- Article
- Identification of a prognosis-related phagocytosis regulator gene signature in medulloblastoma.Heliyon · 2024Article
- Mitochondrial division inhibitor (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism.Scientific reports · 2024Article
- node2vec2rank: Large Scale and Stable Graph Differential Analysis via Multi-Layer Node Embeddings and Ranking.bioRxiv : the preprint server for biology · 2024Article
- HERC5 downregulation in non-small cell lung cancer is associated with altered energy metabolism and metastasis.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite advances in basic and clinical research, metastasis remains the leading cause of death in breast cancer patients. Genetic abnormalities in mitochondria, including mutations affecting complex I and oxidative phosphorylation, are found in breast cancers and might facilitate metastasis. Genes encoding complex I components have significant breast cancer prognostic value. In this study, we used quantitative proteomic analyses to compare a highly metastatic cancer cell line and a parental breast cancer cell line; and observed that NDUFB9, an accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (complex I), was down-regulated in highly metastatic breast cancer cells. Furthermore, we demonstrated that loss of NDUFB9 promotes MDA-MB-231 cells proliferation, migration, and invasion because of elevated levels of mtROS, disturbance of the NAD+/NADH balance, and depletion of mtDNA. We also showed that, the Akt/mTOR/p70S6K signaling pathway and EMT might be involved in this mechanism. Thus, our findings contribute novel data to support the hypothesis that misregulation of mitochondrial complex I NADH dehydrogenase activity can profoundly enhance the aggressiveness of human breast cancer cells, suggesting that complex I deficiency is a potential and important biomarker for further basic research or clinical application.
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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.