ArticleOncogene2022
Disrupted mitochondrial homeostasis coupled with mitotic arrest generates antineoplastic oxidative stress.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
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- Epacadostat and Olaparib Synergistically Inhibit the Growth of BRCA-Proficient Triple-Negative Breast Cancer by Suppressing the Expression of BRCA1 and RAD51.Molecules (Basel, Switzerland) · 2026Article
- Enhancing Escin's Therapeutic Efficacy: A Nanoformulation Approach for Improved Stability and Anticancer Potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Validation of the Mechanism of Action of Jiedu Shengji Oil in the Treatment of Radiation Dermatitis based on Network Pharmacology andCurrent computer-aided drug design · 2026Article
- Excavatolide E triggers oxidative stress-associated apoptosis and DNA damage to inhibit bladder cancer cell proliferation.Molecular biology reports · 2025Article
- Andrographolide Selectively Inhibits the Growth of LA7 Mammary Adenocarcinoma Cells.ACS omega · 2025Article
- Decoding the mechanism for cytotoxicity in thiolato-bridged triosmium carbonyl clusters: from serum reactivity to cellular impact.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2025Article
- Sequential release of MTH1 inhibitor and chemotherapeutic drug using a pH-sensitive polymeric delivery system induces apoptosis in human tongue squamous cell carcinoma CAL-27 cells in vitro.World journal of surgical oncology · 2025Article
- Dysfunctional mitochondria in ageing T cells: a perspective on mitochondrial quality control mechanisms.EMBO reports · 2025Review
- Exploring the therapeutic potential of scorpion venom to mitigate colorectal cancer biomarkers in rats.Journal of the Egyptian National Cancer Institute · 2025Article
- Oxidative and Glycolytic Metabolism: Their Reciprocal Regulation and Dysregulation in Cancer.Cells · 2025Review
- Circular RNA Telomerase Reverses Endothelial Senescence in Progeria.Aging cell · 2025Article
- Multicore, SDS-Based Polyelectrolyte Nanocapsules as Novel Nanocarriers for Paclitaxel to Reduce Cardiotoxicity by Protecting the Mitochondria.International journal of molecular sciences · 2025Article
- Curcumin induces mitochondrial dysfunction-associated oxidative DNA damage in ovarian cancer cells.PloS one · 2025Article
- Disruption of perinatal myeloid niches impacts the aging clock of pancreatic β cells.iScience · 2024Article
- Identification of 3-Aryl-1-benzotriazole-1-yl-acrylonitrile as a Microtubule-Targeting Agent (MTA) in Solid Tumors.International journal of molecular sciences · 2024Article
- Tumor mitochondrial oxidative phosphorylation stimulated by the nuclear receptor RORγ represents an effective therapeutic opportunity in osteosarcoma.Cell reports. Medicine · 2024Article
- Correlation between plasma lycopene levels in patients with laryngeal carcinoma and postoperative adverse complications of chemoradiotherapy and nutritional risks.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) serve as critical signals in various cellular processes. Excessive ROS cause cell death or senescence and mediates the therapeutic effect of many cancer drugs. Recent studies showed that ROS increasingly accumulate during G2/M arrest, the underlying mechanism, however, has not been fully elucidated. Here, we show that in cancer cells treated with anticancer agent TH287 or paclitaxel that causes M arrest, mitochondria accumulate robustly and produce excessive mitochondrial superoxide, which causes oxidative DNA damage and undermines cell survival and proliferation. While mitochondrial mass is greatly increased in cells arrested at M phase, the mitochondrial function is compromised, as reflected by reduced mitochondrial membrane potential, increased SUMOylation and acetylation of mitochondrial proteins, as well as an increased metabolic reliance on glycolysis. CHK1 functional disruption decelerates cell cycle, spares the M arrest and attenuates mitochondrial oxidative stress. Induction of mitophagy and blockade of mitochondrial biogenesis, measures that reduce mitochondrial accumulation, also decelerate cell cycle and abrogate M arrest-coupled mitochondrial oxidative stress. These results suggest that cell cycle progression and mitochondrial homeostasis are interdependent and coordinated, and that impairment of mitochondrial homeostasis and the associated redox signaling may mediate the antineoplastic effect of the M arrest-inducing chemotherapeutics. Our findings provide insights into the fate of cells arrested at M phase and have implications in cancer therapy.
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