ArticleProteomics2013
Oncogene-induced cellular senescence elicits an anti-Warburg effect.
Article in Proteomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Metformin effects on head and neck squamous carcinoma microenvironment: Window of opportunity trial.The Laryngoscope · 2017Trial
- The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming.Nature aging · 2026Article
- The Translatome of Senescent Cells Revealed by Sequencing Actively Translated mRNA.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- Unlocking the Potential of Senolytic Compounds: Advancements, Opportunities, and Challenges in Ageing-Related Research.Sub-cellular biochemistry · 2024Review
- Proteomic characterisation of triple negative breast cancer cells following CDK4/6 inhibition.Scientific data · 2022Article
- Epigenetic Regulation of Cellular Senescence.Cells · 2022Review
- Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021Review
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- Translational Control during Cellular Senescence.Molecular and cellular biology · 2021Review
- Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells.The Journal of biological chemistry · 2019Article
- The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling.Frontiers in aging neuroscience · 2019Review
- Brain Senescence Caused by Elevated Levels of Reactive Metabolite Methylglyoxal on D-Galactose-Induced Aging Mice.Frontiers in neuroscience · 2019Article
- Induction, regulation and roles of neural adhesion molecule L1CAM in cellular senescence.Aging · 2018Article
- Stability of histone post-translational modifications in samples derived from liver tissue and primary hepatic cells.PloS one · 2018Article
- Review
- A Novel Indication for Panobinostat as a Senolytic Drug in NSCLC and HNSCC.Scientific reports · 2017Article
- Detection of the Ubiquitinome in Cells Undergoing Oncogene-Induced Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Apoptotic transition of senescent cells accompanied with mitochondrial hyper-function.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Cellular senescence, an irreversible cell cycle arrest induced by a diversity of stimuli, has been considered as an innate tumor suppressing mechanism with implications and applications in cancer therapy. Using a targeted proteomics approach, we show that fibroblasts induced into senescence by expression of oncogenic Ras exhibit a decrease of global acetylation on all core histones, consistent with formation of senescence-associated heterochromatic foci. We also detected clear increases in repressive markers (e.g. >50% elevation of H3K27me2/3) along with decreases in histone marks associated with increased transcriptional expression/elongation (e.g. H3K36me2/3). Despite the increases in repressive marks of chromatin, 179 loci (of 2206 total) were found to be upregulated by global quantitative proteomics. The changes in the cytosolic proteome indicated an upregulation of mitochondrial proteins and downregulation of proteins involved in glycolysis. These alterations in primary metabolism are opposite to the well-known Warburg effect observed in cancer cells. This study significantly improves our understanding of stress-induced senescence and provides a potential application for triggering it in antiproliferative strategies that target the primary metabolism in cancer cells.
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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.