Estrogen receptor beta (ERbeta) and inhibition of prostate cancer cell proliferation: Studies on the possible mechanism of action in DU145 cells

Pravettoni, A.; Mornati, O.; Martini, Paolo; Marino, Maria; Colciago, Alessandra; Celotti, F.; Motta, Marcella; Negri‐Cesi, P.

doi:10.1016/j.mce.2006.08.008

Cited by 61 publications

(53 citation statements)

References 47 publications

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“…It also decreased the amount of cyclin E, cdc25A, and p45skp2 in T47D breast cancer cells (30). Furthermore, endogenous ERβ is one of the mediators of the antiproliferative action of estrogens in enhancing the synthesis of molecules, such as p21, that control the cell cycle in prostate cancer cells (31). All of these observations indicate that ERβ acts as a tumor suppressor.…”

Section: Discussionmentioning

confidence: 93%

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Feng¹

2011

Oncol Rep

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Abstract. Ovarian clear cell adenocarcinoma (OCCA) is an aggressive ovarian malignancy with a poor prognosis. The role of estrogen receptor β (ERβ) in the development of OCCA remains to be clarified. To investigate the action of ERβ in the proliferation and invasion of OCCA cells, the ES-2 cell line was stably transfected with full-length human ERβ cDNA, and clones were screened and identified using RT-PCR and Western blot assay. ERβ stable transfectants, referred to as ESβ1 and ESβ2 cells, were compared with mock transfectant ESVE and parental ES-2 cells with respect to their growth, motility and ability to activate target genes. ESβ1 and ESβ2 cells expressed ERβ mRNA and protein, whereas ES-2 and ESVE cells were ERβ negative. ERβ transfectants exhibited distinct characteristics from ES-2 and ESVE cells including proliferative properties and the ability to express cyclin D1 in the presence of 17β-estradiol (E 2 ). ERβ inhibited ES-2 cell proliferation, which was determined using the MTT assay, BrdU labeling method and by the down-regulation of cyclin D1 gene expression. Moreover, exogenous ERβ expression resulted in a significant inhibition of ES-2 cell motility in an in vitro invasion assay. ERβ reduced the expression of MMP2 mRNA and the activity of MMP2 enzymatic activity in a ligand-dependent manner. In summary, ERβ may inhibit the proliferation and invasion of ES-2 cells and may be an important regulator in OCCA carcinogenesis.

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Section: Discussionmentioning

confidence: 93%

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Feng¹

2011

Oncol Rep

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“…The two ERs have distinct functions and act antagonistically in multiple pathways: ERa plays an important role in growth and proliferation (Maggiolini et al 2001, Ewan et al 2005, Sun et al 2006, Teng et al 2008 while ERb exerts anti-proliferative, differentiative, and apoptotic actions in breast (Lazennec et al 2001, Paruthiyil et al 2004, Strom et al 2004, prostate (Cheng et al 2004, Pravettoni et al 2007, McPherson et al 2010, Dey et al 2012, and colon cells (Hartman et al 2009, Bielecki et al 2011. Both receptors are required for the maintenance of glucose homeostasis with ERb predominating in the skeletal muscle and ERa in the adipose tissue (Barros et al…”

Section: Physiological and Pathophysiological Actions Of Ersmentioning

confidence: 99%

Insight into the mechanisms of action of estrogen receptor β in the breast, prostate, colon, and CNS

Dey¹,

Barros

Warner

et al. 2013

Journal of Molecular Endocrinology

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Estrogen and its receptors (ERs) influence many biological processes in physiology and pathology in men and women. ERs are involved in the etiology and/or progression of cancers of the prostate, breast, uterus, ovary, colon, lung, stomach, and malignancies of the immune system. In estrogen-sensitive malignancies, ERb usually is a tumor suppressor and ERa is an oncogene. ERb regulates genes in several key pathways including tumor suppression (p53, PTEN); metabolism (PI3K); survival (Akt); proliferation pathways (p45 Skp2 , cMyc, and cyclin E);cell-cycle arresting factors (p21 WAF1

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“…Abiraterone acetate is an orally administered, specific inhibitor of CYP17A1 that has been evaluated in a phase I trial of patients with metastatic CRPC who had undergone multiple hormonal manipulations before enrollment [45]. Significant clinical activity was noted, with PSA reductions of at least 50% occurring in 57% of patients, and symptomatic and radiographic improvement documented in some cases.…”

Section: Novel Approaches In Prostate Cancermentioning

confidence: 99%

Current Medical and Surgical Options for Androgen Deprivation in Prostate Cancer Patients

Bayraktar¹,

A²

2010

TOPCANJ

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Abstract:The growth of prostate cancer cells is driven by androgens. Thus, androgen deprivation, is one of the main treatment modalities in the management of prostate cancer. Historically, bilateral orchiectomy, which achieves 95% reduction of testosterone levels within 3 hours, was the only effective androgen deprivation therapy (ADT). In the 1980s, luteinizing hormone-releasing hormone agonists (LHRH-A) were introduced to reduce testosterone to castration levels. After the 1980s, nonsteroidal antiandrogens were developed in addition to steroidal antiandrogens. Since then, so-called maximum androgen blockade (MAB)/combined androgen blockade (CAB), which is a combination of surgical or medical castration and oral antiandrogens, has been suggested. More recently, novel treatment modalities have been developed, such as intermittent androgen suppression (IAS), nonsteroidal antiandrogen monotherapy, and alternative antiandrogen therapy after relapse from the initial MAB/CAB. ADT, whether surgical or medical, provides important quality of life (QOL) benefits in patients with advanced and metastatic prostate cancer. While the principle of the therapy has remained unchanged, the role, type and timing of these therapies is continuously evolving. This review will focus on the current medical and surgical options for ADT in advanced and metastatic prostate cancer, summarizing the results of several recent clinical trials and discuss their implications for clinical practice and for future research in this disease.

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Estrogen receptor beta (ERbeta) and inhibition of prostate cancer cell proliferation: Studies on the possible mechanism of action in DU145 cells

Cited by 61 publications

References 47 publications

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Insight into the mechanisms of action of estrogen receptor β in the breast, prostate, colon, and CNS

Current Medical and Surgical Options for Androgen Deprivation in Prostate Cancer Patients

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