ReviewMolecular & cellular oncology
Metabolic alterations accompanying oncogene-induced senescence.
Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- "Metabolic memory" of aging: anchoring, transmission, and frontiers of transgenerational intervention.Biogerontology · 2026Review
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.Molecular metabolism · 2024Article
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.bioRxiv : the preprint server for biology · 2024Article
- Eosinophilic Cells in Ovarian Borderline Serous Tumors as a Predictor of BRAF Mutation.Cancers · 2024Article
- NEMO/NF-κB signaling functions as a double-edged sword in PanIN formation versus progression to pancreatic cancer.Molecular cancer · 2024Article
- Senescent Endothelial Cells Sustain Their Senescence-Associated Secretory Phenotype (SASP) through Enhanced Fatty Acid Oxidation.Antioxidants (Basel, Switzerland) · 2023Article
- Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023Review
- Differentially Expressed Circular RNAs and Their Therapeutic Mechanism in Non-segmental Vitiligo Patients Treated With Methylprednisolone.Frontiers in medicine · 2022Article
- Comprehensive Analysis of Immune-Related Metabolic Genes in Lung Adenocarcinoma.Frontiers in endocrinology · 2022Article
- Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Identification and validation of pivotal genes related to age-related meniscus degeneration based on gene expression profiling analysis and in vivo and in vitro models detection.BMC medical genomics · 2021Article
- Radiation-Induced Senescence Reprograms Secretory and Metabolic Pathways in Colon Cancer HCT-116 Cells.International journal of molecular sciences · 2021Article
- Analysis of Age-Related Circular RNA Expression Profiles in Mesenchymal Stem Cells of Rat Bone Marrow.Frontiers in genetics · 2021Article
- Autophagy role(s) in response to oncogenes and DNA replication stress.Cell death and differentiation · 2020Article
- Alteration of fatty acid oxidation by increased CPT1A on replicative senescence of placenta-derived mesenchymal stem cells.Stem cell research & therapy · 2020Article
- AMPK-mediated senolytic and senostatic activity of quercetin surface functionalized FeRedox biology · 2020Article
- The senescent cell epigenome.Aging · 2018Review
- Lipid (per) oxidation in mitochondria: an emerging target in the ageing process?Biogerontology · 2017Review
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 at 1 institution in 1 country.
Funding
Abstract
Senescence is defined as a stable cell growth arrest. Oncogene-induced senescence (OIS) occurs in normal primary human cells after activation of an oncogene in the absence of other cooperating oncogenic stimuli. OIS is therefore considered a bona fide tumor suppression mechanism in vivo. Indeed, overcoming OIS-associated stable cell growth arrest can lead to tumorigenesis. Although cells that have undergone OIS do not replicate their DNA, they remain metabolically active. A number of recent studies report significant changes in cellular metabolism during OIS, including alterations in nucleotide, glucose, and mitochondrial metabolism and autophagy. These alterations may be necessary for stable senescence-associated cell growth arrest, and overcoming these shifts in metabolism may lead to tumorigenesis. This review highlights what is currently known about alterations in cellular metabolism during OIS and the implication of OIS-associated metabolic changes in cellular transformation and the development of cancer therapeutic strategies.
Indexed as
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What OpenQuestion holds
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.