Regulation of Estrogen Receptor Expression in Breast Cancer

Martin, Mary Beth; Saceda, Miguel; Lindsey, Ralph K.

doi:10.1007/978-1-4615-2926-2_11

Cited by 24 publications

(16 citation statements)

References 11 publications

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“…Because ERa levels are known to be downregulated by oestradiol in ER-positive oestrogen-responsive cells (35), it is relevant to investigate whether such regulation still occurs when ER-unresponsive cells overexpress ERa from a transfected gene. Using real-time RT-PCR, ERa mRNA levels were found to be decreased by 8-fold (p-0.001) in 10A-ERa13 cells following 5 days treatment with 10 -8 M 17boestradiol ( Figure 4A).…”

Section: Effect Of 17b-oestradiol On Gene Expression and Growth In Trmentioning

confidence: 99%

Differential effects of overexpression of ERα and ERβ in MCF10A immortalised, non-transformed human breast epithelial cells

Pugazhendhi

Darbre

2009

Hormone Molecular Biology and Clinical Investigation

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Section: Effect Of 17b-oestradiol On Gene Expression and Growth In Trmentioning

confidence: 99%

Differential effects of overexpression of ERα and ERβ in MCF10A immortalised, non-transformed human breast epithelial cells

Pugazhendhi

Darbre

2009

Hormone Molecular Biology and Clinical Investigation

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“…ERα binds to multiple steroid hormone response element half-sites in the ERRα promoter by ChIP assay in MCF-7 breast cancer cells [62]. In contrast, E 2 treatment results in downregulation of ERα in MCF-7 cells [63][64][65][66]. Thus, E 2 treatment alters the molar ratios of ERα and ERRα, thereby changing the relative occupancies of EREs and, consequently, the estrogen responsiveness of other target genes.…”

Section: Errα-mediated Modulation Of Estrogen Responsivenessmentioning

confidence: 99%

Estrogen Receptors as Therapeutic Targets in Breast Cancer

Ariazi¹,

Ariazi²,

Cordera³

et al. 2006

CTMC

255

102

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While estrogen receptor (ER)-targeted therapeutics have clearly been a success in the treatment of breast cancer, the orphan estrogen-related receptors (ERRs) represent novel targets for future development. The ERRs, comprising ERRalpha, ERRbeta and ERRgamma, bind and regulate transcription via estrogen response elements (EREs) and extended ERE half-sites termed ERR response elements (ERREs), but do not bind endogenous estrogens. The emerging role of ERRalpha and ERRgamma in modulating estrogen responsiveness, substituting for ER activities, and serving as prognosticators in breast and other cancers is providing an impetus for the identification of compounds which target these proteins. Moreover, ERRalpha plays a role in energy homeostasis and will likely be targeted for the treatment of metabolic disorders. Multiple classes of synthetic ligands have already been identified. The phytoestrogens genistein, daidzein, biochanin A and 6,3'4'-tryhydroxyflavone have been reported as ERRalpha agonists. The phenolic acyl hydrazones GSK4716 and GSK9089 act as selective agonists of ERRbeta and ERRgamma. The organochlorine pesticides toxaphene and chlordane, and the synthetic compound XCT790 antagonize ERRalpha. The synthetic estrogen diethylstilbestrol antagonizes all three ERRs. The selective estrogen receptor modulators 4-hydroxytamoxifen and 4-hydroxytoremifene antagonize ERRgamma. The rational development of synthetic ligands for the ERRs may soon provide new agents to supplement the repertoire of antihormonal therapies to combat breast cancer. Moreover, expression of ERRs in other cancers and metabolic disorders may provide a targeted treatment strategy for these patients as well.

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“…In addition, Saceda et al (1988) and Martin et al (1993) have shown that OE2 regulates ER through suppression of ER mRNA in a human breast cancer cell line . Their data suggest that OE2 suppresses ER mRNA by the inhibition of ER gene transcription at early times after addition and also by a post-transcriptional effect on ER mRNA at later times.…”

Section: Introductionmentioning

confidence: 97%

Effect of oestradiol-17β on the expression of oestrogen receptor mRNA in human tonsillar cells

Evagelatou

Farrant²

1995

Journal of Molecular Endocrinology

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We have investigated the expression of oestrogen receptor (ER) mRNA in Ficoll-separated tonsillar cells and the changes that occur with the addition of oestradiol (OE2) both in the presence and the absence of the T cell mitogen phytohaemagglutinin (PHA). The amounts of ER mRNA and beta-actin mRNA in the samples were determined by slot blotting and hybridization and quantified by densitometry. The levels of ER mRNA were normalized against the beta-actin mRNA content. In the presence of OE2 (7 x 10(-8) M) after a 10-h culture there was a significant decrease (P < 0.05) to about 66% of the control (0-h culture) ER mRNA levels. Stimulating the cultures with PHA (1 microgram/ml), without the presence of OE2, had no effect on the expression of ER mRNA. However, when OE2 was present in a 10-h culture of PHA-stimulated cells, the ER mRNA level was significantly decreased (P < 0.05) to about 60% of control levels. In 24-h cultures, the presence of OE2 and/or PHA had no effect. When separated T cell preparations from the tonsils were used, no significant effects of OE2 were seen in either the 10-h or 24-h cultures. In conclusion, OE2 downregulates the ER mRNA content in a tonsillar mononuclear cell system in vitro as it does in many primary oestrogen target cells.

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Regulation of Estrogen Receptor Expression in Breast Cancer

Cited by 24 publications

References 11 publications

Differential effects of overexpression of ERα and ERβ in MCF10A immortalised, non-transformed human breast epithelial cells

Differential effects of overexpression of ERα and ERβ in MCF10A immortalised, non-transformed human breast epithelial cells

Estrogen Receptors as Therapeutic Targets in Breast Cancer

Effect of oestradiol-17β on the expression of oestrogen receptor mRNA in human tonsillar cells

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