2006
DOI: 10.1038/sj.onc.1209565
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Identification of an ataxia telangiectasia-mutated protein mediated surveillance system to regulate Bcl-2 overexpression

Abstract: Bcl-2 can both promote and attenuate tumorigenesis. Although the former function is relatively well characterized, the mechanism of the latter remains elusive. We report here that enforced Bcl-2 expression in MCF7 cells stabilizes p53, induces phosphorylation of p53 serine 15 (p53pSer15) and inhibits MCF7 cell growth. Consistent with p53 Ser15 being a target of ataxia telangiectasia mutated protein(ATM)/ATR (ATM-and rad3-related) in the DNA damage response, Bcl-2 activates ATM by inducing ATM Ser1981 phosphory… Show more

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Cited by 3 publications
(3 citation statements)
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“…Several covariate mechanisms are responsible for multi-drug resistance in breast cancer cells including increased drug efflux (P-glycoprotein-P-gp), CSCs (CD24), drug detoxification (glutathione S-transferase) deregulated apoptosis (Bcl-2 overexpression) and overexpression of cytokines (SCF ) [8]. The anti-apoptotic expression of Bcl-2 is well documented and its affects on tumourigenic activity [14]. CD24 is a phenotypic surface marker for granulocytes, Bcl’s and CSCs, which are implicated in resistance to both chemotherapy and radiotherapy.…”
Section: Discussionmentioning
confidence: 99%
“…Several covariate mechanisms are responsible for multi-drug resistance in breast cancer cells including increased drug efflux (P-glycoprotein-P-gp), CSCs (CD24), drug detoxification (glutathione S-transferase) deregulated apoptosis (Bcl-2 overexpression) and overexpression of cytokines (SCF ) [8]. The anti-apoptotic expression of Bcl-2 is well documented and its affects on tumourigenic activity [14]. CD24 is a phenotypic surface marker for granulocytes, Bcl’s and CSCs, which are implicated in resistance to both chemotherapy and radiotherapy.…”
Section: Discussionmentioning
confidence: 99%
“…Consistent with this conclusion, unchallenged t(14:18) cells, which express high levels of Bcl-2, show spontaneous, high levels of g-H2AX foci (present data and ref. 44). The significance of these points is underscored by the fact that the presence of DSB and activation of DNA damage signaling are detected in precancerous tissues, interpreted as a consequence of endogenous replication stress, and proposed as initial events of tumorigenesis (45,46).…”
Section: Bcl-2 Represses Hr Via Retention Of Brca1 In Organellesmentioning
confidence: 99%
“…Since tamoxifen exhibits antiestrogenic activities in breast cancer cells, this study indicated that tamoxifen up-regulated the expression of ERα and exerted its antagonistic effect through ERα in MCF-7 cells [24]. Although bcl-2 is an anti-apoptotic protein that inhibits apoptosis, it has also been reported to be involved in the surveillance of oncogenesis and the suppression of tumorigenesis [25]. Therefore, the up-regulation of bcl-2 gene may explain the effect of tamoxifen in decreasing cell proliferation in MCF-7 cells.…”
mentioning
confidence: 94%