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      Loss of androgen receptor expression promotes a stem-like cell phenotype in prostate cancer through STAT3 signaling.

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          Abstract

          Androgen receptor (AR) signaling is important for prostate cancer progression. However, androgen-deprivation and/or AR targeting-based therapies often lead to resistance. Here, we demonstrate that loss of AR expression results in STAT3 activation in prostate cancer cells. AR downregulation further leads to development of prostate cancer stem-like cells (CSC), which requires STAT3. In human prostate tumor tissues, elevated cancer stem-like cell markers coincide with those cells exhibiting high STAT3 activity and low AR expression. AR downregulation-induced STAT3 activation is mediated through increased interleukin (IL)-6 expression. Treating mice with soluble IL-6 receptor fusion protein or silencing STAT3 in tumor cells significantly reduced prostate tumor growth and CSCs. Together, these findings indicate an opposing role of AR and STAT3 in prostate CSC development.

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          Author and article information

          Journal
          Cancer Res.
          Cancer research
          1538-7445
          0008-5472
          Feb 15 2014
          : 74
          : 4
          Affiliations
          [1 ] Authors' Affiliations: Departments of Molecular Medicine, Cancer Immunotherapy and Tumor Immunology, and Medical Oncology, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Duarte, California; and Institute for Biochemistry and Molecular Biology, Universitätsklinikum RWTH Aachen, Aachen, Germany.
          Article
          0008-5472.CAN-13-0594 NIHMS535664
          10.1158/0008-5472.CAN-13-0594
          4539262
          24177177
          5c2dd4ad-77a0-4bb6-83e9-95a791447c59
          ©2013 AACR.
          History

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