ReviewInternational journal of molecular sciences2025
Dysregulation of Mitochondrial Function in Cancer Cells.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed.
- Metabolic Reprogramming of Cancer Stem Cells: Targeting Lipid Flux and Mitochondrial Plasticity to Overcome Therapeutic Resistance.Cancer medicine · 2026Review
- Deciphering the Multiscale Morphology of Somatic Oncogenic Alterations in Hepatocellular Carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Research progress on VDAC2 in mitochondrial dysfunction-related diseases.Molecular biology reports · 2026Review
- ATP5F1B promotes breast cancer progression through ERK associated metabolic reprogramming.Molecular biology reports · 2026Article
- The linker governs the organelle targeting of TPP⁺-modified zinc phthalocyanine photosensitizers.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Review
- Review
- N-Acetylneuraminate Pyruvate Lyase Promotes Cell Adaptation to Glucose Deprivation by Regulating Intracellular ATP Levels.Current issues in molecular biology · 2026Article
- Mitochondrial oxidative phosphorylation inhibition by 9α,11α-dihydroxy-kaurenoic acid promotes ROS-associated apoptosis and suppresses cancer stemness in non-small cell lung cancer.Scientific reports · 2026Article
- The FGD5-AS1/miR-142-5p/CDK5 axis promotes ESCC progression by regulating mitochondrial fission and mitophagy: insights from integrative bioinformatics and experimental analyses.World journal of surgical oncology · 2026Article
- Synergistic Anti-Tumor Activity of LRPPRC Inhibition and Dasatinib Through Dual Oxidative Phosphorylation Disruption.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Mitochondrial Long Non-Coding RNAs in Gynecological Cancers: Pathogenic Signaling Pathways and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Next Generation Calcium Nanomaterials: Disrupting Tumor CaInternational journal of nanomedicine · 2026Review
- Mechanistic insights and challenges in mitochondrial regulation of macrophage polarization and inflammatory responses.Frontiers in physiology · 2026Review
- Selegiline, a monoamine oxidase-B inhibitor as a modulator of metabolic reprogramming for cancer therapy: a review.Frontiers in pharmacology · 2026Review
- Chronically Established ρJournal of Cancer · 2026Article
- Mitochondria: from powerhouses of cells to hubs in antitumor immunity.Frontiers in immunology · 2026Review
- Targeted phytotherapy: essential oils, multi-target cancer action & nanodelivery.Frontiers in oncology · 2026Review
- Integrating single-cell transcriptomics and whole-genome CRISPR CAS9 screen identifies a cell cluster associated with tumor dependency in triple-negative breast cancer.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to their well-known role in ATP production, mitochondria are vital to cancer cell metabolism due to their involvement in redox regulation, apoptosis, calcium signaling, and biosynthesis. This review explores how cancer cells drive the extensive reprogramming of mitochondrial structure and function, enabling malignant cells to survive hostile microenvironments, evade therapy, and proliferate rapidly. While glycolysis (the Warburg effect) was once thought to be the dominant force behind cancer metabolism, recent updates underscore the pivotal contribution of mitochondrial oxidative phosphorylation (OXPHOS) to tumor development. Cancer cells often exhibit enhanced mitochondrial ATP production, metabolic flexibility, and the ability to switch between energy sources such as glucose, glutamine, and pyruvate. Equally important are changes in mitochondrial morphology and dynamics. Due to disruptions in fusion and fission processes, regulated by proteins like Drp1 and MFN1/2, cancer cells often display fragmented mitochondria, which are linked to increased motility, metastasis, and tumor progression. Moreover, structural mitochondrial alterations not only contribute to drug resistance but may also serve as biomarkers for therapeutic response. Emerging evidence also points to the influence of oncometabolites and retrograde signaling in reshaping mitochondrial behavior under oncogenic stress. Collectively, these insights position mitochondria as central regulators of cancer biology and attractive targets for therapy. By unraveling the molecular mechanisms underlying mitochondrial reprogramming-from energy production to structural remodeling-researchers can identify new approaches to disrupt cancer metabolism and enhance treatment efficacy.
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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.