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- W4361253062 abstract "<div>Abstract<p>Decreased <i>BRCA1</i> expression in the absence of genetic mutation is observed frequently in sporadic cancers of the breast and other sites, although little is known regarding the mechanisms by which the expression of this gene can be repressed. Here, we show that activating and repressive E2Fs simultaneously bind the <i>BRCA1</i> promoter at two adjacent E2F sites <i>in vivo</i>, and that hypoxia induces a dynamic redistribution of promoter occupancy by these factors resulting in the transcriptional repression of <i>BRCA1</i> expression. Functionally, we show that hypoxia is associated with impaired homologous recombination, whereas the nonhomologous end-joining (NHEJ) repair pathway is unaffected under these conditions. Repression of <i>BRCA1</i> expression by hypoxia represents an intriguing mechanism of functional <i>BRCA1</i> inactivation in the absence of genetic mutation. We propose that hypoxia-induced decreases in <i>BRCA1</i> expression and consequent suppression of homologous recombination may lead to genetic instability by shifting the balance between the high-fidelity homologous recombination pathway and the error-prone NHEJ pathway of DNA repair. Furthermore, these findings provide a novel link between E2Fs and the transcriptional response to hypoxia and provide insight into the mechanisms by which the tumor microenvironment can contribute to genetic instability in cancer. (Cancer Res 2005; 65(24): 11597-604)</p></div>" @default.
- W4361253062 created "2023-03-31" @default.
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- W4361253062 date "2023-03-30" @default.
- W4361253062 modified "2023-09-29" @default.
- W4361253062 title "Data from Hypoxia-Induced Down-regulation of <i>BRCA1</i> Expression by E2Fs" @default.
- W4361253062 doi "https://doi.org/10.1158/0008-5472.c.6494678" @default.
- W4361253062 hasPublicationYear "2023" @default.
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