Detection of Estrogen Receptor-Beta mRNA in Breast Cancer Using RT-PCR

Cullen, R.; Maguire, Teresa; Diggin, P.; Hill, A. D. K.; McDermott, Enda; O’Higgins, N.; Duffy, Michael J.

doi:10.1177/172460080001500122

Cited by 4 publications

(4 citation statements)

References 5 publications

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“…The reason for the different mitogenic effects exerted by E2 in colon cancer and breast cancer cells may reside in the expression of different estrogen receptors in the two cell lines. In this regard, we demonstrated that HT29 colonocytes express mainly ER , supporting previous observations (Arai et al 2000), whereas MCF-7 cells express mainly ER , as in previously reported findings (Cullen et al 2000). Further, ER and ER have different roles in the transcription regulation of various genes.…”

Section: Discussionsupporting

confidence: 79%

“…In support of these hypotheses, different responses to AP1-activation sites exerted by ER and ER have been described by Paech et al (1997). Moreover, gene expression of ER in colorectal mucosa has been described (Arai et al 2000, Campbell-Thompson et al 2001), but ER is detected at very low levels in breast cancer tissues, according to our and others findings (Cullen et al 2000). These observations led us to suggest a functional implication for ER in estrogen's mediation of VDR expression in colonic cells.…”

Section: Discussionsupporting

confidence: 63%

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Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Gilad

Bresler²,

J³

et al. 2005

Journal of Endocrinology

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We previously demonstrated that 17 -estradiol (E2) regulates the transcription and expression of the vitamin D receptor (VDR) in rat colonocytes and duodenocytes in vivo. The aim of the present study was to assess whether the extracellular signal-regulated kinase (ERK) induced by E2 is involved in regulating VDR expression. We compared E2-associated signaling activity in HT29 colon cancer cells, a non-classical E2-target, with that in MCF-7 breast cancer cells, the natural targets of the hormone. E2 did not affect proliferation of HT29 cells, but enhanced proliferation of MCF-7 cells. Vitamin D inhibited proliferation of both cell lines and the combined treatment induced potentiation of vitamin D activity. E2 upregulated VDR transcription and protein expression concomitantly with ERK 1/2 phosphorylation in both cell lines. PD98059, a specific mitogen-activated protein kinase (MAPK) inhibitor, prevented E2-mediated activation of ERK 1/2, with concomitant inhibition of VDR expression. ICI182780 inhibited VDR expression in HT29 and MCF-7 cell lines. A conjugate of E2 and bovine serum albumin upregulated phosphorylation of ERK 1/2 and concomitantly enhanced VDR expression in a similar fashion as the nonconjugated hormone. Expression of ER and ER was detected in MCF-7 and HT29 cell lines respectively, which localized to the nuclei, cytosol and caveolar membrane rather than non-caveolar membrane. Disruption of lipid rafts/caveolae by depleting cellular cholesterol with the cholesterol-binding reagentmethylcyclodextrin blocked ERK 1/2 phosphorylation concomitantly with VDR upregulation. The tyrosine phosphorylation inhibitor suramin and src kinase inhibitor PP2 inhibited both ERK 1/2 phosphorylation and VDR expression. E2 induced phosphorylation of Raf and Jun in a time-dependent manner. The Ras/Raf dependent inhibitor of transactivation sulindac sulfide also blocked E2 effects. The specific c-Jun phosphorylation inhibitor SP600125 dose dependently inhibited c-Jun phosphorylation and VDR expression. The MAPK/ERK kinase inhibitor PD 98059 downregulated both c-Jun phosphorylation and VDR expression indicating that upstream and downstream events in the signaling cascade are all related to the control of VDR expression. Taken together, our data suggest that E2 binds to receptors compartmentalized to membranal caveolar domains in HT29 and MCF-7 cells, inducing ERK 1/2 activation and transcriptional activity, which finally results in upregulation of expression of the VDR gene.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 63%

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Gilad

Bresler²,

J³

et al. 2005

Journal of Endocrinology

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“…In general, both receptors display similar ligand-binding profiles, but phytoestrogens like genistein and coumestrol induce receptor-dependent transcription stronger with ER␤ than with ER␣ [8,9]. Furthermore, the tissue distribution of ER␣ and ER␤ also differs substantially [8,10]. ER␤ is very important in the bone, urogenital tract, cardiovascular system, central nervous system and the developing brain [11,12].…”

Section: Introductionmentioning

confidence: 96%

Rapid yeast estrogen bioassays stably expressing human estrogen receptors α and β, and green fluorescent protein: a comparison of different compounds with both receptor types

Bovee¹,

Helsdingen²,

Rietjens

et al. 2004

The Journal of Steroid Biochemistry and Molecular Biology

180

151

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“…In 1996 it became evident that one major player in the story, the second ER, ERβ, had gone unnoticed (Kuiper et al 1996) and that its presence may well have some bearing on the development and treatment of hormone-dependent cancers. ERβ is highly expressed in the prostate (Kuiper et al 1996) and is expressed together with ERα in both normal and malignant breasts (Dotzlaw et al 1997, Vladusic et al 1998, Fuqua et al 1999, Speirs et al 1999, Cullen et al 2000, Iwao et al 2000, Jarvinen et al 2000, Speirs & Kerin 2000, Omoto et al 2001, Roger et al 2001. It is, therefore, not surprising that a great deal of interest is focused on the role of ERβ in normal and malignant growth of these two organs.…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor beta in breast cancer.

Palmieri

Cheng²,

Saji³

et al. 2002

Endocrine-Related Cancer

218

136

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Estrogen is essential for normal growth and differentiation in the mammary gland. It also supports growth of approximately 50% of primary breast cancers. For this reason, removal of estrogen or blocking of its action with the anti-estrogen, tamoxifen, is the main treatment for estrogen receptor alpha (ERα)-positive tumors. In 1996, when oncologists became aware of a second ER, ERβ, there was some doubt as to whether this receptor would be of importance in breast cancer because the clinical consensus was that responsiveness to tamoxifen is related to the presence of ERα in breast cancer. Today we know that ERα and ERβ have distinct cellular distributions, regulate separate sets of genes and can oppose each other's actions on some genes. We also know that ERβ is widely expressed in both the normal and malignant breast and that there are proliferating cells in the breast which express ERβ. In this review we summarize what is known about ERβ in breast cancer and examine the possibility that ERβ-selective ligands may well represent a useful class of pharmacological tools with a novel target, namely proliferating cells expressing ERβ.

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Detection of Estrogen Receptor-Beta mRNA in Breast Cancer Using RT-PCR

Cited by 4 publications

References 5 publications

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Rapid yeast estrogen bioassays stably expressing human estrogen receptors α and β, and green fluorescent protein: a comparison of different compounds with both receptor types

Estrogen receptor beta in breast cancer.

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