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• W2089803053 abstract "Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DCThe escape from tumor dormancy has been shown to be mediated by the acquisition of the angiogenic phenotype. Utilizing an in vivo model that reliably recapitulates the transition from the preangiogenic to the angiogenic phenotype, we have identified and validated the differential expression of a number of genes including a basic leucine zipper transcription factor, ATF-like-3 (BATF3). We further found that the mRNA level of BATF3 is significantly upregulated in angiogenic tumor lesions compared to preangiogenic lesions. In order to investigate the role of BATF3 in breast cancer neovascularization, we established a panel of ER+ and ER- breast cancer cell lines, MCF7 and MDA-MB-231, respectively, which stably overexpress BATF3 by lentiviral transduction. Cells overexpressing BATF3 exhibited significantly increased levels of VEGF (vascular endothelial growth factor) compared to their wild type counterparts. Overexpression of BATF3 also significantly increased cell invasion in both cell lines. Moreover, MMP-9 (Matrix Metalloproteinase-9) levels and activity were significantly increased in MDA-MB-231-BATF3 cells. This latter observation suggested that the increased invasiveness observed might be due to elevated levels of MMP-9, which has been shown to regulate tumor cell invasion by remodeling the surrounding extracellular matrix. TIMP-1, an endogenous inhibitor of MMP-9 activity, was also significantly increased in MDA-MB-231-BATF3 cells, however the ratio of MMP-9 to TIMP-1 is dramatically higher in these cells as compared with control cells. Interestingly, BATF3 also significantly suppressed cell proliferation in both the MDA-MB-231 and MCF7 cell lines. Taken together, these data support the conclusion that BATF3 may play a dual role in the regulation of tumor angiogenesis, growth and progression. (Supported by NIH P01 CA045548, The Breast Cancer Research Foundation, The Advanced Medical Research Foundation, and the Harvard College Research Program).Citation Format: Elliot Stein, Di Jia, Marsha Moses. BATF3 is a novel regulator of breast cancer cell invasion. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3892. doi:10.1158/1538-7445.AM2013-3892" @default.
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• W2089803053 date "2013-04-15" @default.
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• W2089803053 title "Abstract 3892: BATF3 is a novel regulator of breast cancer cell invasion." @default.
• W2089803053 doi "https://doi.org/10.1158/1538-7445.am2013-3892" @default.
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