ArticleJournal of cellular and molecular medicine2011
Cutting edge: Chk1 directs senescence and mitotic catastrophe in recovery from G₂ checkpoint arrest.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- 5G RF-EMFs Mitigate UV-Induced Genotoxic Stress Through Redox Balance and p38 Pathway Regulation in Skin Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Inactivation of the SLC25A1 gene during embryogenesis induces a unique senescence program controlled by p53.Cell death and differentiation · 2025Article
- Heterogenous Differences in Cellular Senescent Phenotypes in Pre-Eclampsia and IUGR following Quantitative Assessment of Multiple Biomarkers of Senescence.International journal of molecular sciences · 2023Article
- PIDD1 in cell cycle control, sterile inflammation and cell death.Biochemical Society transactions · 2022Review
- A novel M phase blocker, DCZ3301 enhances the sensitivity of bortezomib in resistant multiple myeloma through DNA damage and mitotic catastrophe.Journal of experimental & clinical cancer research : CR · 2020Article
- Analysis of centrosome and DNA damage response in PLK4 associated Seckel syndrome.European journal of human genetics : EJHG · 2017Article
- Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.Neoplasia (New York, N.Y.) · 2017Article
- The Ubiquitin-like with PHD and Ring Finger Domains 1 (UHRF1)/DNA Methyltransferase 1 (DNMT1) Axis Is a Primary Regulator of Cell Senescence.The Journal of biological chemistry · 2017Article
- Chk1 Promotes DNA Damage Response Bypass following Oxidative Stress in a Model of Hydrogen Peroxide-Associated Ulcerative Colitis through JNK Inactivation and Chromatin Binding.Oxidative medicine and cellular longevity · 2017Article
- Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.Biological research · 2016Article
- PKCι depletion initiates mitotic slippage-induced senescence in glioblastoma.Cell cycle (Georgetown, Tex.) · 2015Article
- SUV39H1 downregulation induces deheterochromatinization of satellite regions and senescence after exposure to ionizing radiation.Frontiers in genetics · 2014Article
- Repeated H2 O2 exposure drives cell cycle progression in an in vitro model of ulcerative colitis.Journal of cellular and molecular medicine · 2013Article
- ATF2 knockdown reinforces oxidative stress-induced apoptosis in TE7 cancer cells.Journal of cellular and molecular medicine · 2013Article
- Non-apoptotic function of caspases in a cellular model of hydrogen peroxide-associated colitis.Journal of cellular and molecular medicine · 2013Article
- Radiation-induced cellular senescence results from a slippage of long-term G2 arrested cells into G1 phase.Cell cycle (Georgetown, Tex.) · 2013Article
- DNA damage signaling induced by the G-quadruplex ligand 12459 is modulated by PPM1D/WIP1 phosphatase.Nucleic acids research · 2013Article
- Death-associated protein kinase controls STAT3 activity in intestinal epithelial cells.The American journal of pathology · 2013Article
- P53-dependent antiproliferative and pro-apoptotic effects of trichostatin A (TSA) in glioblastoma cells.Journal of neuro-oncology · 2012Article
- Spontaneous cellular senescence and stress response heterogeneity in human vestibular schwannomas.Neuro-oncology advancesArticle
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Besides the well-understood DNA damage response via establishment of G(2) checkpoint arrest, novel studies focus on the recovery from arrest by checkpoint override to monitor cell cycle re-entry. The aim of this study was to investigate the role of Chk1 in the recovery from G(2) checkpoint arrest in HCT116 (human colorectal cancer) wt, p53(-/-) and p21(-/-) cell lines following H(2) O(2) treatment. Firstly, DNA damage caused G(2) checkpoint activation via Chk1. Secondly, overriding G(2) checkpoint led to (i) mitotic slippage, cell cycle re-entry in G(1) and subsequent G(1) arrest associated with senescence or (ii) premature mitotic entry in the absence of p53/p21(WAF1) causing mitotic catastrophe. We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle. Thus, G(2) arrest correlated with downstream senescence, but late G(2) arrest led to mitotic catastrophe, although both cell cycle re-entries were linked to upstream Chk1 signalling. Chk1 knockdown deciphered that Chk1 defines long-term DNA damage responses causing cell cycle re-entry. We propose that recovery from oxidative DNA damage-induced G(2) arrest requires Chk1. It works as cutting edge and navigates cells to senescence or mitotic catastrophe. The decision, however, seems to depend on p53/p21(WAF1) . The general relevance of Chk1 as an important determinant of recovery from G(2) checkpoint arrest was verified in HT29 colorectal 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.