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      The Role of Androgen Receptor Signaling in Ovarian Cancer

      review-article
      Author(s): 1 , 2 , 3 , 1 , 2 , 4 , *
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: androgen, androgen receptor, carcinogenesis, ovary, tumor progression

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          Abstract

          Emerging evidence has suggested that androgen receptor signaling plays an important role in ovarian cancer outgrowth. Specifically, androgen receptor activation appears to be associated with increased risks of developing ovarian cancer and inducing tumor progression. However, conflicting findings have also been reported. This review summarizes and discusses the available data indicating the involvement of androgens as well as androgen receptor and related signals in ovarian carcinogenesis and cancer growth. Although the underlying molecular mechanisms for androgen receptor functions in ovarian cancer remain far from being fully understood, current observations may offer effective chemopreventive and therapeutic approaches, via modulation of androgen receptor activity, against ovarian cancer. Indeed, several clinical trials have been conducted to determine the efficacy of androgen deprivation therapy in patients with ovarian cancer.

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          AIB1, a steroid receptor coactivator amplified in breast and ovarian cancer.

          S Anzick, J Kononen, R L Walker … (1997)
          Members of the recently recognized SRC-1 family of transcriptional coactivators interact with steroid hormone receptors to enhance ligand-dependent transcription. AIB1, a member of the SRC-1 family, was cloned during a search on the long arm of chromosome 20 for genes whose expression and copy number were elevated in human breast cancers. AIB1 amplification and overexpression were observed in four of five estrogen receptor-positive breast and ovarian cancer cell lines. Subsequent evaluation of 105 unselected specimens of primary breast cancer found AIB1 amplification in approximately 10 percent and high expression in 64 percent of the primary tumors analyzed. AIB1 protein interacted with estrogen receptors in a ligand-dependent fashion, and transfection of AIB1 resulted in enhancement of estrogen-dependent transcription. These observations identify AIB1 as a nuclear receptor coactivator whose altered expression may contribute to development of steroid-dependent cancers.
          Article 0 comments Cited 184 times – based on 0 reviews     Review now
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            The length and location of CAG trinucleotide repeats in the androgen receptor N-terminal domain affect transactivation function.

            N L Chamberlain, E D Driver, R L Miesfeld (1994)
            Some transcription factors contain stretches of polyglutamine encoded by repeats of the trinucleotide CAG. Expansion of the CAG repeat in the androgen receptor (AR) has been correlated with the incidence and severity of X-linked spinal and bulbar muscular atrophy (Kennedy's disease). In order to understand the relationship of this mutation to AR function, we constructed ARs that varied in the position and size of the polyglutamine tract, and assayed for the abilities of these mutant receptors to bind androgen and to activate transcription of several different AR-responsive reporter genes. Elimination of the tract in both human and rat AR resulted in elevated transcriptional activation activity, strongly suggesting that the presence of the polyglutamine tract is inhibitory to transactivation. Progressive expansion of the CAG repeat in human AR caused a linear decrease of transactivation function. Importantly, expansion of the tract did not completely eliminate AR activity. We postulate that this residual AR activity may be sufficient for development of male primary and secondary sex characteristics, but may fall below a threshold level of activity necessary for normal maintenance of motor neuron function. This functional abnormality may be representative of other genetic diseases that are associated with CAG expansion mutations in open reading frames, such as spinocerebellar ataxia type I and Huntington's disease.
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              The RAB25 small GTPase determines aggressiveness of ovarian and breast cancers.

              Karen Smith-McCune, Kyosuke Yamada, Nelly Auersperg … (2004)
              High-density array comparative genomic hybridization (CGH) showed amplification of chromosome 1q22 centered on the RAB25 small GTPase, which is implicated in apical vesicle trafficking, in approximately half of ovarian and breast cancers. RAB25 mRNA levels were selectively increased in stage III and IV serous epithelial ovarian cancers compared to other genes within the amplified region, implicating RAB25 as a driving event in the development of the amplicon. Increased DNA copy number or RNA level of RAB25 was associated with markedly decreased disease-free survival or overall survival in ovarian and breast cancers, respectively. Forced expression of RAB25 markedly increased anchorage-dependent and anchorage-independent cell proliferation, prevented apoptosis and anoikis, including that induced by chemotherapy, and increased aggressiveness of cancer cells in vivo. The inhibition of apoptosis was associated with a decrease in expression of the proapoptotic molecules, BAK and BAX, and activation of the antiapoptotic phosphatidylinositol 3 kinase (PI3K) and AKT pathway, providing potential mechanisms for the effects of RAB25 on tumor aggressiveness. Overall, these studies implicate RAB25, and thus the RAB family of small G proteins, in aggressiveness of epithelial cancers.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 19 February 2019
                Publication date Collection: February 2019
                Volume: 8
                Issue: 2
                Electronic Location Identifier: 176
                Affiliations
                [1 ]Department of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA; mizu123shima@ 123456gmail.com
                [2 ]James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY 14642, USA
                [3 ]Department of Obstetrics and Gynecology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan
                [4 ]Department of Urology, University of Rochester Medical Center, Rochester, NY 14642, USA
                Author notes
                [* ]Correspondence: hiroshi_miyamoto@ 123456urmc.rochester.edu ; Tel.: +1-585-275-8748; Fax: +1-585-273-3637
                Author information
                https://orcid.org/0000-0002-3505-4717
                https://orcid.org/0000-0001-7610-7769
                Article
                Publisher ID: cells-08-00176
                DOI: 10.3390/cells8020176
                PMC ID: 6406955
                PubMed ID: 30791431
                SO-VID: e2ef778b-1ef9-4042-b1c7-f63f1290a97c
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 28 January 2019
                Date accepted : 16 February 2019
                Categories
                Subject: Review

                Keywords: androgen,androgen receptor,carcinogenesis,ovary,tumor progression
                Data availability:
                Keywords: androgen, androgen receptor, carcinogenesis, ovary, tumor progression

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