2012
DOI: 10.18632/aging.100512 View full text |Buy / Rent full text
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Abstract: The down-regulation of dominant oncogenes, including C-MYC, in tumor cells often leads to the induction of senescence via mechanisms that are not completely identified. In the current study, we demonstrate that MYC-depleted melanoma cells undergo extensive DNA damage that is caused by the underexpression of thymidylate synthase (TS) and ribonucleotide reductase (RR) and subsequent depletion of deoxyribonucleoside triphosphate pools. Simultaneous genetic inhibition of TS and RR in melanoma cells induced DNA dam… Show more

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“…1 and 2; Table 1), which corroborates with data from recent studies that show RRM2 is overexpressed in EOCs. 35,36 RRM2 upregulation is sufficient to overcome the senescence-associated cell growth arrest tumor suppression mechanism, [23][24][25][26] implying that RRM2 may drive proliferation of transformed cells. Indeed, we observed that RRM2 expression positively correlates with the expression of the cell proliferation marker Ki67 (Table 1).…”
Section: Discussionmentioning
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“…1 and 2; Table 1), which corroborates with data from recent studies that show RRM2 is overexpressed in EOCs. 35,36 RRM2 upregulation is sufficient to overcome the senescence-associated cell growth arrest tumor suppression mechanism, [23][24][25][26] implying that RRM2 may drive proliferation of transformed cells. Indeed, we observed that RRM2 expression positively correlates with the expression of the cell proliferation marker Ki67 (Table 1).…”
Section: Discussionmentioning
“…16,22,42 These results are consistent with previous reports from our lab and others. [23][24][25][26] Cisplatin, which is the primary front-line chemotherapy used for EOC, 5 also induces DNA damage. 43 Therefore, it is interesting to speculate whether there might be synergism between RRM2 inhibition and cisplatin treatment to increase the DNA damage to a threshold beyond which senescence would occur.…”
Section: Discussionmentioning
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“…This is a stable growth arrest that occurs when an activated oncogene is expressed in a normal cell. Mannava et al 96,97 found that human fibroblasts undergoing OIS induced by HRAS-G12V or MYC expression underexpressed both RNR and thymidylate synthase and contained low dNTP pools. Ectopic expression of the two enzymes restored dNTP pools and suppressed senescence-associated phenotypes.…”
Section: Transversion Mutagenesismentioning
“…Interestingly, a similar role of dNTP pools in control of DNA damage and senescence phenotypes was shown in melanoma cells undergoing senescence due to depletion of C-MYC oncogene. 80 SSB engage serine/threonine-protein kinase ATR (ataxia telangiectasia and Rad3-related protein), which activates checkpoint kinase 1 (CHK1). CHK1, in turn, phosphorylates CDC25, one of the key regulators of cell cycle progression, causing its degradation.…”
Section: G12vmentioning