Abstract
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 DNAbinding 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.
Keywords: Cancer, cell signaling, FAK1, focal adhesion, metastasis, Pax-5, B lymphopoiesis, cell differentiation, homeostasis, leukemia
Anti-Cancer Agents in Medicinal Chemistry
Title: Coordinated Expression of Pax-5 and FAK1 in Metastasis
Volume: 11 Issue: 7
Author(s): Nicolas Crapoulet, Pierre O'Brien, Rodney J. Ouellette and Gilles A. Robichaud
Affiliation:
Keywords: Cancer, cell signaling, FAK1, focal adhesion, metastasis, Pax-5, B lymphopoiesis, cell differentiation, homeostasis, leukemia
Abstract: 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 DNAbinding 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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Cite this article as:
Crapoulet Nicolas, O'Brien Pierre, J. Ouellette Rodney and A. Robichaud Gilles, Coordinated Expression of Pax-5 and FAK1 in Metastasis, Anti-Cancer Agents in Medicinal Chemistry 2011; 11 (7) . https://dx.doi.org/10.2174/187152011796817637
DOI https://dx.doi.org/10.2174/187152011796817637 |
Print ISSN 1871-5206 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5992 |
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