Novel role of BRCA1 interacting C‐terminal helicase 1 (<i>BRIP1</i>) in breast tumour cell invasion
<p dir="ltr">Breast cancer (BC) is the most common malignancy and the leading cause of death in women worldwide. Only 5%-10% of mutations in BRCA genes are associated with familial breast tumours in Eastern countries, suggesting the contribution of other genes. Using a microarray gen...
محفوظ في:
| المؤلف الرئيسي: | |
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| مؤلفون آخرون: | , , |
| منشور في: |
2020
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| الموضوعات: | |
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إضافة وسم
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| الملخص: | <p dir="ltr">Breast cancer (BC) is the most common malignancy and the leading cause of death in women worldwide. Only 5%-10% of mutations in BRCA genes are associated with familial breast tumours in Eastern countries, suggesting the contribution of other genes. Using a microarray gene expression profiling study of BC, we have recently identified <i>BRIP1</i> (fivefold up-regulation) as a potential gene associated with BC progression in the Omani population. Although <i>BRIP1</i> regulates DNA repair and cell proliferation, the precise role of <i>BRIP1</i> in BC cell invasion/metastasis has not been explored yet; this prompted us to test the hypothesis that <i>BRIP1</i> promotes BC cell proliferation and invasion. Using a combination of cellular and molecular approaches, our results revealed differential overexpression of <i>BRIP1</i> in different BC cell lines. Functional assays validated further the physiological relevance of <i>BRIP1</i> in tumour malignancy, and siRNA-mediated <i>BRIP1</i> knockdown significantly reduced BC cell motility by targeting key motility-associated genes. Moreover, down-regulation of <i>BRIP1</i> expression significantly attenuated cell proliferation via cell cycle arrest. Our study is the first to show the novel function of <i>BRIP1</i> in promoting BC cell invasion by regulating expression of various downstream target genes. Furthermore, these findings provide us with a unique opportunity to identify <i>BRIP1</i>-induced pro-invasive genes that could serve as biomarkers and/or targets to guide the design of appropriate BC targeted therapies.</p><h2>Other Information</h2><p dir="ltr">Published in: Journal of Cellular and Molecular Medicine<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="http://dx.doi.org/10.1111/jcmm.15761" target="_blank">http://dx.doi.org/10.1111/jcmm.15761</a></p> |
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