期刊
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
卷 11, 期 7, 页码 643-649出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/187152011796817637
关键词
Cancer; cell signaling; FAK1; focal adhesion; metastasis; Pax-5
资金
- Atlantic Innovation Foundation
- New Brunswick Innovation Foundation
- Beatrice Hunter Cancer Research Institute
- Canadian Institutes of Health Research (CIHR)
The Pax-5 gene encodes a B-cell-specific activator protein (BSAP) that plays a key role in B lymphocyte differentiation and embryogenesis. The deregulation of this transcription factor is also linked to B cell malignancies and recently to other cancers. More specifically, the downstream effects of Pax-5 promote cell-cell interactions and mediate the activation of adhesion genes which result in an epithelial phenotypic behavior of human carcinoma cells. To gain a better understanding of Pax-5-mediated gene regulation, we studied available gene expression data in depth and identified several Pax-5 downstream targets. Among these, we found that Pax-5 activity is consistently inversely correlated with the expression of Focal Adhesion Kinase 1 (FAK1). FAK1 is known to enhance migration of cancer cells and promote metastatic dissemination to distant sites. Further analysis looking at genome wide profiling of Pax-5 DNA-binding points to both direct and indirect regulation of FAK1 expression by Pax-5 and its downstream targets. These findings suggest a key role for Pax-5 in phenotypic transitioning during metastasis through the regulation of FAK1 activity.
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