ArticleMolecular and cellular biology2009
Mitochondrial dysfunction contributes to oncogene-induced senescence.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 1 of them a synthesis that pooled it.
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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
193 citing papers in PubMed, 1 synthesis or guideline pooled it, 387 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Quantitative proteomics reveals coordinated changes in the proteome during replicative senescence.Nature communications · 2026Article
- Review
- CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression.iScience · 2026Article
- Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.BMB reports · 2026Review
- Hypoxia Preserves Chromatin Integrity and Delays Cellular Senescence through Epigenetic Regulation.Biomolecules & therapeutics · 2026Review
- Mitochondrial bioenergetics-SASP crosstalk determines senolytic efficacy in therapy-induced senescence.Cell death discovery · 2026Article
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Aging-associated transcriptional programming of mitochondrial respiration in alveolar type II epithelial cells.Frontiers in cell and developmental biology · 2026Article
- Reactive Oxygen Species: Molecular Mechanisms, Cellular Targets, and Implications for Genomic Stability.BioMed research international · 2026Review
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Review
- Downregulation of Sod2 increases atypical flat lesions and dysplasia to advance pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Targeting PON2 with Vutiglabridin Restores Mitochondrial Integrity and Attenuates Oxidative Stress-Induced Senescence.Antioxidants (Basel, Switzerland) · 2025Article
- Biological and translational attributes of mitochondrial DNA copy number: Laboratory perspective to clinical relevance.World journal of methodology · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- A lncRNA-mediated metabolic rewiring of cell senescence.Cell reports · 2025Article
- NHE7 drives endometrial cancer progression by delaying senescence through cAMP/CREB/GRIN2B axis-mediated Ca²⁺ influx.Communications biology · 2025Article
- ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation.Nature communications · 2025Article
- Recent Anti-KRASCancers · 2025Review
133 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of oncogenic ras in normal human cells quickly induces an aberrant proliferation response that later is curtailed by a cell cycle arrest known as cellular senescence. Here, we show that cells expressing oncogenic ras display an increase in the mitochondrial mass, the mitochondrial DNA, and the mitochondrial production of reactive oxygen species (ROS) prior to the senescent cell cycle arrest. By the time the cells entered senescence, dysfunctional mitochondria accumulated around the nucleus. The mitochondrial dysfunction was accompanied by oxidative DNA damage, a drop in ATP levels, and the activation of AMPK. The increase in mitochondrial mass and ROS in response to oncogenic ras depended on intact p53 and Rb tumor suppression pathways. In addition, direct interference with mitochondrial functions by inhibiting the expression of the Rieske iron sulfur protein of complex III or the use of pharmacological inhibitors of the electron transport chain and oxidative phosphorylation was sufficient to trigger senescence. Taking these results together, this work suggests that mitochondrial dysfunction is an effector pathway of oncogene-induced senescence.
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Registered trials
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.