ArticleOncogene2010
Prevention of premature senescence requires JNK regulation of Bcl-2 and reactive oxygen species.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- The Association Between Serum Gamma-Glutamyl Transferase and Gastrointestinal Cancer Risk: A Systematic Review and Meta-Analysis.Cancer medicine · 2025Pooled it
- Review
- Deprivation of EGFR signal causes senolysis in PDAC with CDK4/6 inhibition.Cell death and differentiation · 2026Article
- Senescence and senolysis in cancer: The latest findings.Cancer science · 2024Review
- Integrated Stress Response (ISR) Pathway: Unraveling Its Role in Cellular Senescence.International journal of molecular sciences · 2023Review
- c-Jun N-terminal kinase signaling in cellular senescence.Archives of toxicology · 2023Review
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Involvement of Bcl-2 Family Proteins in Tetraploidization-Related Senescence.International journal of molecular sciences · 2023Review
- In Vitro Anticancer Activity of Novel Ciprofloxacin Mannich Base in Lung Adenocarcinoma and High-Grade Serous Ovarian Cancer Cell Lines via Attenuating MAPK Signaling Pathway.Molecules (Basel, Switzerland) · 2023Article
- The landscape of aging.Science China. Life sciences · 2022Review
- STING mediates nuclear PD-L1 targeting-induced senescence in cancer cells.Cell death & disease · 2022Article
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
- The FOXO signaling axis displays conjoined functions in redox homeostasis and stemness.Free radical biology & medicine · 2021Review
- The Paradoxical Role of Cellular Senescence in Cancer.Frontiers in cell and developmental biology · 2021Review
- Reply.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- JNK Pathway as a Target for Osteoarthritis: Comment on the Article by Loeser et al.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Deletion of JNK Enhances Senescence in Joint Tissues and Increases the Severity of Age-Related Osteoarthritis in Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- JNK Signaling in Stem Cell Self-Renewal and Differentiation.International journal of molecular sciences · 2020Review
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Phosphoregulation on mitochondria: Integration of cell and organelle responses.CNS neuroscience & therapeutics · 2019Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Premature senescence is considered as a cellular defense mechanism to prevent tumorigenesis. Although recent evidences show that c-Jun N-terminal kinase (JNK) is involved in the senescence process, the mechanism for this regulation is not fully understood. Here, we examined the role of JNK in premature senescence of tumor cells. Treatment of cells with the JNK-specific inhibitor SP600125 caused phenotypical changes of senescence and triggered a rapid increase in mitochondrial reactive oxygen species (ROS) production and DNA-damage response (DDR) in MCF7 breast carcinoma cells. ROS generation was attributed to the suppression of B-cell lymphoma-2 (Bcl-2) phosphorylation, and resulted in DNA damage and p53 activation. Bax did not change their localization to the mitochondria, which is required for apoptosis. The essential roles of JNK and phosphorylated Bcl-2 in preventing premature senescence were confirmed using RNA interference and ectopic expression of mutants of Bcl-2, including phosphomimetic and nonphosphorylatable forms. These findings were evidenced in H460 lung carcinoma cells and primary human embryonic fibroblasts. Altogether, our results showed that loss of JNK activity triggers a Bcl-2/ROS/DDR signaling cascade that ultimately leads to premature senescence, indicating that basal JNK activity is essential in preventing premature senescence.
Indexed as
Identifiers
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.