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Aberrant BAF57 Signaling Facilitates Prometastatic Phenotypes
Journal article   Open access   Peer reviewed

Aberrant BAF57 Signaling Facilitates Prometastatic Phenotypes

Sucharitha Balasubramaniam, Clay E. S. Comstock, Adam Ertel, Kwang Won Jeong, Michael R. Stallcup, Sankar Addya, Peter A. McCue, William F. Ostrander, Michael A. Augello and Karen E. Knudsen
Clinical cancer research, v 19(10), pp 2657-2667
15 May 2013
PMID: 23493350
url
https://doi.org/10.1158/1078-0432.ccr-12-3049View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1158/1078-0432.CCR-12-3049View
Published, Version of Record (VoR) Open

Abstract

Life Sciences & Biomedicine Oncology Science & Technology
Purpose: BAF57, a component of the switching-defective and sucrose nonfermenting (SWI/SNF) chromatin-remodeling complex conglomerate, modulates androgen receptor activity to promote prostate cancer. However, the molecular consequences of tumor-associated BAF57 expression have remained undefined in advanced disease such as castration-resistant prostate cancer and/or metastasis. Experimental Design: Clinical human specimens of primary and metastatic prostate cancer were immunohistochemically examined for tumor-grade association of BAF57 expression. Global gene expression analyses were conducted in models mimicking tumor-associated BAF57 expression. Aberrant BAF57-dependent gene expression changes, bypass of androgen-mediated signaling, and chromatin-specific SWI/SNF complex alterations with respect to cytoskeletal remodelers such as integrins were validated. Cell migration assays were used to profile the biologic phenotypes conferred under conditions simulating tumor-derived BAF57 expression. Results: Immunohistochemical quantitation of primary human specimens revealed that BAF57 was significantly and aberrantly elevated as a function of tumor grade. Critically, gene expression analyses showed that BAF57 deregulation circumvented androgen-mediated signaling, elicited alpha 2 integrin upregulation, and altered other SWI/SNF complex components at the alpha 2 integrin locus. BAF57-dependent alpha 2 integrin induction conferred a prometastatic migratory advantage, which was attenuated by anti-alpha 2 integrin antibody blockade. Furthermore, BAF57 was found to be markedly upregulated in human prostate cancer metastases of the lung, lymph node, and dura. Conclusion: The findings herein, identifying tumor-associated BAF57 perturbation as a means to bypass androgen- signaling events that facilitate novel prometastatic phenotypes, link BAF57 upregulation to tumor dissemination. These data thereby establish BAF57 as a putative marker of metastatic potential that could be leveraged for therapeutic intervention. (C) 2013 AACR.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Oncology
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