Estrogen Receptor β mRNA in Colon Cancer Cells: Growth Effects of Estrogen and Genistein

Arai, Naoya; Ström, Anders; Rafter, Joseph; Gustafsson, Jan Åke

doi:10.1006/bbrc.2000.2444

Cited by 119 publications

(81 citation statements)

References 30 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: 92%

“…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: Discussionmentioning

confidence: 76%

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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: 92%

Section: Discussionmentioning

confidence: 76%

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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“…The basal expression of DFNA5 in CRC cell lines (HCT116, HT29, DLD-1, and SW480) was also undetectable or very low [11], but these CRC cell lines express ER mRNA (β-isoform) [14,15]. Interestingly, DFNA5 methylation was found only in ER-positive cell lines.…”

Section: Discussionmentioning

confidence: 98%

Methylation of the DFNA5 increases risk of lymph node metastasis in human breast cancer

Kim

Lebron

Nagpal

et al. 2008

Biochemical and Biophysical Research Communications

126

123

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The pathogenesis of breast cancer involves multiple genetic and epigenetic events. In this study, we report an epigenetic alteration of DFNA5 in human breast cancer. DFNA5 gene was silenced in breast cancer cell lines that were methylated in the DFNA5 promoter, and restored by treatment with the demethylating agent, 5-aza-dC, and gene knock-down of DFNA5 increased cellular invasiveness in vitro. The mRNA expression of DFNA5 in breast cancer tissues was downregulated as compared to normal tissues. Moreover, the DFNA5 promoter was found to be methylated in primary tumor tissues with high frequency (53%, 18/34). Quantitative methylationspecific PCR of DFNA5 clearly discriminated primary breast cancer tissues from normal breast tissues (15.3%, 2/13). Moreover, methylation status of DFNA5 was correlated with lymph node metastasis in breast cancer patients. Our data implicate DFNA5 promoter methylation as a novel molecular biomarker in human breast cancer. Keywords DFNA5; The human deafness; Autosomal dominant 5 gene; Promoter methylation; Breast cancerAlthough breast cancer mortality declined significantly in recent years, in part due to early diagnosis by screening mammography, the limitations of mammography are wellrecognized [1,2]. Therefore, novel approaches for the early detection of breast cancer are necessary. The pathogenesis of breast cancer involves multiple genetic and epigenetic events. In spite of recent advances in the assessment of breast cancer risk, the identification of crucial susceptibility genes such as BRCA1/2, PTEN, and p53 account for only about 5% of all breast cancer cases [3]. The marked cytogenetic complexity seen in advanced breast cancer precludes investigators from readily identifying primary causative genetic and epigenetic events in breast cell carcinogenesis [4].

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“…Another reason is the different expressions of ERβ isoforms in CRC. There are at least 5 different ERβ isoforms, which show different amino acid sequences at the COOH terminus and are differently expressed in tumor cell lines [31][32][33][34][35] . Campbell-Thompson et al [35] and Witte et al [36] showed that ERβ was the predominant ER subtype between human colon and that the decreased levels of ERβ1 and ERβ2 mRNA were associated with colonic tumorigenesis in females.…”

Section: Discussionmentioning

confidence: 99%

Expression of estrogen receptor ® in human colorectal cancer

Xie¹,

Yu²,

Luo³

2004

WJG

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Estrogen Receptor β mRNA in Colon Cancer Cells: Growth Effects of Estrogen and Genistein

Cited by 119 publications

References 30 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

Methylation of the DFNA5 increases risk of lymph node metastasis in human breast cancer

Expression of estrogen receptor ® in human colorectal cancer

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