ArticleCellular & molecular biology letters2014
Decay of γ-H2AX foci correlates with potentially lethal damage repair and P53 status in human colorectal carcinoma cells.
Article in Cellular & molecular biology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
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- Loss of miR-101-3p in melanoma stabilizes genomic integrity, leading to cell death prevention.Cellular & molecular biology letters · 2024Article
- Twist1 induces chromosomal instability (CIN) in colorectal cancer cells.Human molecular genetics · 2020Article
- Effect of X-ray minibeam radiation therapy on clonogenic survival of glioma cells.Clinical and translational radiation oncology · 2018Article
- Acquired resistance to tyrosine kinase inhibitors may be linked with the decreased sensitivity to X-ray irradiation.Oncotarget · 2018Article
- Screening of Pleural Mesotheliomas for DNA-damage Repair Players by Digital Gene Expression Analysis Can Enhance Clinical Management of Patients Receiving Platin-Based Chemotherapy.Journal of Cancer · 2016Article
- Lung microenvironment promotes the metastasis of human hepatocellular carcinoma cells to the lungs.International journal of clinical and experimental medicine · 2015Article
- Radiation oncology in vitro: trends to improve radiotherapy through molecular targets.BioMed research international · 2014Review
- MiR-101 induces senescence and prevents apoptosis in the background of DNA damage in MCF7 cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The influence of p53 status on potentially lethal damage repair (PLDR) and DNA double-strand break (DSB) repair was studied in two isogenic human colorectal carcinoma cell lines: RKO (p53 wild-type) and RC10.1 (p53 null). They were treated with different doses of ionizing radiation, and survival and the induction of DNA-DSB were studied. PLDR was determined by using clonogenic assays and then comparing the survival of cells plated immediately with the survival of cells plated 24 h after irradiation. Doses varied from 0 to 8 Gy. Survival curves were analyzed using the linear-quadratic formula: S(D)/S(0) = exp-(αD+βD(2)). The γ-H2AX foci assay was used to study DNA DSB kinetics. Cells were irradiated with single doses of 0, 0.5, 1 and 2 Gy. Foci levels were studied in non-irradiated control cells and 30 min and 24 h after irradiation. Irradiation was performed with gamma rays from a (137)Cs source, with a dose rate of 0.5 Gy/min. The RKO cells show higher survival rates after delayed plating than after immediate plating, while no such difference was found for the RC10.1 cells. Functional p53 seems to be a relevant characteristic regarding PLDR for cell survival. Decay of γ-H2AX foci after exposure to ionizing radiation is associated with DSB repair. More residual foci are observed in RC10.1 than in RKO, indicating that decay of γ-H2AX foci correlates with p53 functionality and PLDR in RKO cells.
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