Potential of endogenous estrogen receptor β to influence the selective ER modulator ERβ complex

Cui, Bin; Gajdos, Csaba; Dardes, Rita C.; Kidwai, Noman; Johnston, Stephen; Dowsett, Mitchell; Jordan, V. Craig

doi:10.3892/ijo.27.2.327

Cited by 3 publications

(4 citation statements)

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“…42,43 In this study, we show ERβ was unable to interact with CK8 or CK18, a prerequisite for receptor immobilization to the nuclear matrix and subsequent degradation. An altered ratio of ERα to ERβ has been reported in fulvestrant resistant breast cancer cells, 42 supporting the notion that ERβ may contribute to fulvestrant resistance.…”

Section: Methodsmentioning

confidence: 70%

Estrogen receptor-alpha-interacting cytokeratins potentiate the antiestrogenic activity of fulvestrant

Long

Fan

Nephew

2010

Cancer Biology & Therapy

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Section: Methodsmentioning

confidence: 70%

Estrogen receptor-alpha-interacting cytokeratins potentiate the antiestrogenic activity of fulvestrant

Long

Fan

Nephew

2010

Cancer Biology & Therapy

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“…At 10 lM TAM, MDA-MB-231 cell growth was decreased to 17% of controls and MCF-7 growth was decreased to 7% of controls. Although MDA-MB-231 cells are reported to be estrogen receptor alpha-negative, they do express small but detectable levels of estrogen receptor beta [24]. Thus, it is possible the inhibition of MDA-MB-231 cell growth by TAM may be being mediated by estrogen receptor beta or TAM may be acting to inhibit growth by means in addition to its role as an antiestrogen.…”

Section: Tam Inhibits Growth Of Mcf-7 and Mda-mb-231 Cellsmentioning

confidence: 95%

“…MCF-7 and MDA-MB-231 breast cancer cell lines were chosen for this study. MCF-7 cells are estrogen receptor- Previous research has indicated that SIT has growth inhibitory effects on MCF-7 and MDA-MB-231 breast cancer cells [14,15,24] and on tumors of other organs (e. g., prostate and colon) [26 -28] in vitro and in vivo. This effect may be mediated by the proapoptotic effect of SIT [14,16].…”

Section: Discussionmentioning

confidence: 99%

β‐Sitosterol enhances tamoxifen effectiveness on breast cancer cells by affecting ceramide metabolism

Awad

Barta

Fink

et al. 2008

Molecular Nutrition Food Res

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The objective of this study was to investigate the effects of the dietary phytosterol beta-sitosterol (SIT) and the antiestrogen drug tamoxifen (TAM) on cell growth and ceramide (CER) metabolism in MCF-7 and MDA-MB-231 human breast cancer cells. The MCF-7 and MDA-MB-231 cell lines were studied as models of estrogen receptor positive and estrogen receptor negative breast cancer cells. Growth of both cell lines as determined using the sulforhodamine B assay was inhibited by treatment with 16 microM SIT but only MCF-7 cell growth was inhibited by treatment with 1 microM TAM. The combination of SIT and TAM further inhibited growth in both cell lines, most significantly in MDA-MB-231 cells. CER is a proapoptotic signal and CER levels were increased in both MCF-7 and MDA-MB-231 cells by individual treatment with SIT and TAM and the combined treatment raised cellular CER content even further. SIT and TAM raised CER levels by different means. SIT potently activated de novo CER synthesis in both MCF-7 and MDA-MB-231 cells by stimulating serine palmitoyltransferase activity; whereas TAM promoted CER accumulation in both cell types by inhibiting CER glycosylation. These results suggest that the combination regimen of dietary SIT and TAM chemotherapy may be beneficial in the management of breast cancer patients.

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“…Prior to the development of reliable ERβ antibodies, studies using RNA extracted from heterogeneous tissue extracts showed that coexpression of both ER subtypes was associated with poor prognosis and elevated expression of ERβ correlated with tamoxifen resistance [85,86]. More recent studies have refuted this, showing no change in ERβ mRNA between tamoxifen-naïve and tamoxifenstimulated cell lines [87], while over-expression of ERβ in MCF-7 cells did not result in tamoxifen resistance but instead led to increased sensitivity to tamoxifen [88]. Antibody-based studies on clinical samples have shown that ERα-positive breast tumours which express low levels of ERβ tend to be refractory to tamoxifen [53,89,90].…”

Section: Erα and -β And Hormone Resistancementioning

confidence: 99%

New perspectives into the biological and clinical relevance of oestrogen receptors in the human breast

Speirs

Walker

2007

The Journal of Pathology

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Oestrogen receptor (ER) is arguably the single most important biological predictive factor that exists today. In the last 10 years or so, however, our understanding of ER biology has undergone a paradigm shift following the identification of a second ER, ERbeta, with the original ER being renamed ERalpha. A number of isoforms have additionally been described, especially for ERbeta. Our knowledge of ER signalling has also increased with the recognition of accessory co-regulatory proteins, which help direct the transcriptional cascade. Here we outline these changes and discuss what biological and clinical implications these could have in the mammary gland.

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Potential of endogenous estrogen receptor β to influence the selective ER modulator ERβ complex

Cited by 3 publications

References 0 publications

Estrogen receptor-alpha-interacting cytokeratins potentiate the antiestrogenic activity of fulvestrant

Estrogen receptor-alpha-interacting cytokeratins potentiate the antiestrogenic activity of fulvestrant

β‐Sitosterol enhances tamoxifen effectiveness on breast cancer cells by affecting ceramide metabolism

New perspectives into the biological and clinical relevance of oestrogen receptors in the human breast

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