Expression profiling of the mouse prostate after castration and hormone replacement: implication of H-cadherin in prostate tumorigenesis

Wang, Xi-De; Wang, Bu-Er; Soriano, Robert; Zha, Jiping; Zhang, Zemin; Modrušan, Zora; Cunha, Gerald R.; Gao, Wei‐Qiang

doi:10.1111/j.1432-0436.2006.00135.x

Cited by 58 publications

(57 citation statements)

References 63 publications

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“…To test this hypothesis, we evaluated the gene expression profiles of intact and castrated mouse prostate tissue using microarray analysis (GDS2562; ref. 23). Consistent with this hypothesis, we found that the expression of N-cadherin, Zeb1, Twist1, and Slug were upregulated 3 days after castration and continued to increase over time (Fig.…”

Section: Resultssupporting

confidence: 85%

Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy

Sun¹,

Wang²,

Leong³

et al. 2012

Cancer Research

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318

315

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Androgen deprivation is currently a standard-of-care, first-line therapy for prostate cancer in the United States. Although this regimen effectively regresses androgen-dependent disease, relapse often occurs in an androgenindependent manner and is associated with poor prognosis. Such castration-resistant prostate cancer represents a major clinical challenge, and the mechanisms underlying castration resistance are not fully understood. Epithelial-mesenchymal transition (EMT) is a key developmental process and has also been implicated in cancer metastasis and therapeutic resistance in recent years. However, the factors contributing to EMT in human cancers remain unclear. Here, we show that both normal mouse prostate tissue and human LuCaP35 prostate tumor explants display an EMT as well as increased stem cell-like features following androgen deprivation. Importantly, we observed similar changes in mesenchymal features in prostate tumors from patients treated with androgen-deprivation therapy. In addition, we have delineated a feedback loop involving the androgen receptor and the Zeb1 transcription factor that seems to mediate this transition. In summary, we show for the first time that androgen deprivation induces EMT in both normal prostate and prostate cancer, revealing a potentially important consequence of a standard-of-care treatment for prostate cancer. This finding could have significant implications for second-line treatment strategies in this clinical setting. Cancer Res; 72(2); 527-36. Ó2011 AACR.

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Section: Resultssupporting

confidence: 85%

Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy

Sun¹,

Wang²,

Leong³

et al. 2012

Cancer Research

Self Cite

318

315

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“…Highly invasive growth pattern (Berx et al 1998) Up-regulated expression Epithelial ovarian cancer (Sato et al 1998;Maruyama et al 2001;Toyooka et al 2001;Toyooka et al 2002;Roman-Gomez et al 2003;Hibi et al 2004;Sakai et al 2004;Kim et al 2005;Wang et al 2007;Brock et al 2008;Jin et al 2008;Yan et al 2008) LOH and promoter methylation Ovary Skin (BCC and SCC) Diffuse large B cell lymphoma HCC Tumor invasion; increased cell proliferation and resistance to apoptosis (Kawakami et al 1999;Takeuchi et al 2002a;Takeuchi et al 2002b;Ogama et al 2004;Chan et al 2008) Expression in intratumoral endothelium…”

Section: Somatic Mutations Breast (Ilc) Gastric (Dgc) Pancreasmentioning

confidence: 99%

Involvement of Members of the Cadherin Superfamily in Cancer

Berx¹,

Roy²

2009

Cold Spring Harbor Perspectives in Biology

564

489

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We review the role of cadherins and cadherin-related proteins in human cancer. Cellular and animal models for human cancer are also dealt with whenever appropriate. E-cadherin is the prototype of the large cadherin superfamily and is renowned for its potent malignancy suppressing activity. Different mechanisms for inactivating E-cadherin/CDH1 have been identified in human cancers: inherited and somatic mutations, aberrant protein processing, increased promoter methylation, and induction of transcriptional repressors such as Snail and ZEB family members. The latter induce epithelial mesenchymal transition, which is also associated with induction of "mesenchymal" cadherins, a hallmark of tumor progression. VE-cadherin/CDH5 plays a role in tumor-associated angiogenesis. The atypical T-cadherin/ CDH13 is often silenced in cancer cells but up-regulated in tumor vasculature. The review also covers the status of protocadherins and several other cadherin-related molecules in human cancer. Perspectives for emerging cadherin-related anticancer therapies are given.

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“…Several genome-wide studies in mice have shed some light on the AR-regulated program in benign prostate tissue. Wang et al (2007) profiled gene expression by microarray in the mouse after castration and hormone replacement, finding that most significantly regulated genes were involved in cell adhesion, metabolism, and cell-cycle progression. Pritchard et al (2009) profiled gene expression in the mouse prostate at seven time points, from prostate induction through branching morphogenesis, to full adult secretory differentiation.…”

Section: Ar In Prostate Cancer Initiationmentioning

confidence: 99%

Androgens and androgen receptor signaling in prostate tumorigenesis

Zhou¹,

Bolton²,

Jones³

2014

Journal of Molecular Endocrinology

164

112

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Androgens and androgen receptor (AR) signaling are necessary for prostate development and homeostasis. AR signaling also drives the growth of nearly all prostate cancer cells. The role of androgens and AR signaling has been well characterized in metastatic prostate cancer, where it has been shown that prostate cancer cells are exquisitely adept at maintaining functional AR signaling to drive cancer growth. As androgens and AR signaling are so intimately involved in prostate development and the proliferation of advanced prostate cancer, it stands to reason that androgens and AR are also involved in prostate cancer initiation and the early stages of cancer growth, yet little is known of this process. In this review, we summarize the current state of knowledge concerning the role of androgens and AR signaling in prostate tissue, from development to metastatic, castration-resistant prostate cancer, and use that information to suggest potential roles for androgens and AR in prostate cancer initiation.

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Expression profiling of the mouse prostate after castration and hormone replacement: implication of H-cadherin in prostate tumorigenesis

Cited by 58 publications

References 63 publications

Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy

Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy

Involvement of Members of the Cadherin Superfamily in Cancer

Androgens and androgen receptor signaling in prostate tumorigenesis

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