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- W2000897752 abstract "Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DCPrevious reports suggest that, besides its therapeutic effects, ionizing radiation (IR) may increase the invasiveness of surviving cancer cells. Here, we show that this activity of IR in lung cancer cells is mediated by a signaling pathway that involves p38 kinase, phosphoinositide 3-kinase, Akt, and MMP-2. The invasion-promoting doses of IR also increased and reduced the levels of vimentin and E-cadherin, respectively, both of which are markers for the epithelial-mesenchymal transition (EMT). Interestingly, all these actions of IR were mimicked by the overexpression of Bcl-XL in lung cancer cells. Moreover, both RNA and protein levels of Bcl-XL were elevated upon irradiation of the cells, and the prevention of this event using small interfering RNAs of Bcl-XL reduced the ability of IR to promote invasion signals and EMT-associated events. This suggests that Bcl-XL functions as a signaling mediator of the malignant effects of IR. It was also demonstrated that IR enhances levels of STAT3 phosphorylation, and the reduction of STAT3 levels by RNA interference prevented IR-induced Bcl-XL accumulation, and thus all the tested Bcl-XL-dependent events. Overall, the data suggest that IR induces Bcl-XL accumulation via STAT3, which then promotes cancer cell invasion and EMT-associated markers. Our findings demonstrate a novel function of Bcl-XL in cancer, and also advance our understanding of the malignant actions of IR significantly.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5274." @default.
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- W2000897752 date "2010-04-15" @default.
- W2000897752 modified "2023-09-25" @default.
- W2000897752 title "Abstract 5274: Role of Bcl-XLand STAT3 in γ-irradiation-induced invasion of lung cancer cells" @default.
- W2000897752 doi "https://doi.org/10.1158/1538-7445.am10-5274" @default.
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