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• W2068133362 endingPage "1439" @default.
• W2068133362 startingPage "1424" @default.
• W2068133362 abstract "Cells respond to genotoxic stress by activating the DNA damage response (DDR). When injury is severe or irreparable, cells induce apoptosis or cellular senescence to prevent transmission of the lesions to the daughter cells upon cell division. Resistance to apoptosis is a hallmark of cancer that challenges the efficacy of cancer therapy. In this work, the effects of ionizing radiation on apoptosis-resistant E1A + E1B transformed cells were investigated to ascertain whether the activation of cellular senescence could provide an alternative tumor suppressor mechanism. We show that irradiated cells arrest cell cycle at G 2/M phase and resume DNA replication in the absence of cell division followed by formation of giant polyploid cells. Permanent activation of DDR signaling due to impaired DNA repair results in the induction of cellular senescence in E1A + E1B cells. However, irradiated cells bypass senescence and restore the population by dividing cells, which have near normal size and ploidy and do not express senescence markers. Reversion of senescence and appearance of proliferating cells were associated with downregulation of mTOR, activation of autophagy, mitigation of DDR signaling, and expression of stem cell markers." @default.
• W2068133362 created "2016-06-24" @default.
• W2068133362 creator A5006150559 @default.
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• W2068133362 creator A5060051766 @default.
• W2068133362 creator A5086583788 @default.
• W2068133362 creator A5088411994 @default.
• W2068133362 date "2014-03-07" @default.
• W2068133362 modified "2023-10-10" @default.
• W2068133362 title "Sustained activation of DNA damage response in irradiated apoptosis-resistant cells induces reversible senescence associated with mTOR downregulation and expression of stem cell markers" @default.
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• W2068133362 doi "https://doi.org/10.4161/cc.28402" @default.
• W2068133362 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4050140" @default.
• W2068133362 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24626185" @default.
• W2068133362 hasPublicationYear "2014" @default.
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