The different roles of ER subtypes in cancer biology and therapy

Thomas, Christoforos; Gustafsson, Jan‐Åke

doi:10.1038/nrc3093

Cited by 574 publications

(581 citation statements)

References 164 publications

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“…Recent studies have indicated that the efficacy of endocrine therapy cannot be simply explained by the expression levels of ERα, but may be determined by the expression profiles of both ERα and ERβ, as well as their various splice variants (14,21,24,25). Furthermore, to understand the meaning of the demonstrated change in ERα-36 expression induced by BMP2 in breast cancer cells, additional research should be carried out to determine whether the ERα-36 reported in the present study is the same as that reported by Wang et al (21).…”

Section: Discussionmentioning

confidence: 99%

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Induction of estrogen receptor α-36 expression by bone morphogenetic protein 2 in breast cancer cell lines

Wang

Huang

Baowei

et al. 2012

Molecular Medicine Reports

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Abstract. The expression of estrogen receptor-α (ERα) is one of the most important diagnostic and prognostic factors of breast cancer. Recently, ERα-36 has been identified as a novel variant of ER-α. ERα-36 lacks intrinsic transcription activity and mainly mediates non-genomic estrogen signaling. Bone morphogenetic proteins (BMPs) are recognized as key factors during the control of cell fate and cancer development. However, the correlation between BMP and the ER signaling pathway remains unclear. In this study, we show that BMP2, a member of the BMP family, is a novel inducer of ERα-36 expression in breast cancer cells. As shown by western blot assays, the upregulation of ERα-36 by BMP2 was significant. In MDA-MB-231 cells which are ERα-66-negative, BMP2 was able to induce the expression of ERα-36 in a dose-dependent manner, and the RNA interference assay indicated a correlation between BMP2 and ERα-36 expression. BMP2 inhibited the growth of MCF-7 and MDA-MB-231 cells; however, the inhibitory effect was antagonized by tamoxifen, suggesting that the ER signal was involved. The growth of MDA-MB-231 cells was stimulated by 17-β-estradiol (E2) after BMP2 induction, even though the cells were previously insensitive to E2. These results suggest that BMP2 induces ERα-36 expression and alters tumor resistance to endocrine therapy by changing the expression profile of ERs.

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Section: Discussionmentioning

confidence: 99%

“…The ER signaling pathway plays a pivotal role in the development of different types of breast cancer (14). Two types of ERs have been identified, ERα and ERβ, both of which have many mRNA splice variants (15).…”

Section: Introductionmentioning

confidence: 99%

Induction of estrogen receptor α-36 expression by bone morphogenetic protein 2 in breast cancer cell lines

Wang

Huang

Baowei

et al. 2012

Molecular Medicine Reports

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“…However, E2 effects in mammals include the regulation of growth and differentiation of several organs and tissues influencing the whole homeostasis maintenance in both male and female organisms (Thomas and Gustafsson 2011). Thus, Nar ability to interfere with ER activities raises some concerns on the putative unhealthy side effects of this flavonoid.…”

Section: Introductionmentioning

confidence: 99%

“…Although adult skeletal muscle is a stable tissue, it possesses the remarkable ability to rapidly recover and regenerate following injury (Thomas and Gustafsson 2011;Hawke and Garry 2001). In response to injury, undifferentiated satellite cells are activated from a quiescent state and proliferate as myoblasts.…”

Section: Introductionmentioning

confidence: 99%

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

et al. 2014

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Several experiments sustain healthful benefits of the flavanone naringenin (Nar) against chronic diseases including its protective effects against estrogen-related cancers. These experiments encourage Nar use in replacing estrogen treatment in post-menopausal women avoiding the serious side effects ascribed to this hormone. However, at the present, scarce data are available on the impact of Nar on E2-regulated cell functions. This study was aimed at determining the impact of Nar on the estrogen receptor (ERa and b)-dependent signals important for 17b-estradiol (E2) effect in muscle cells (rat L6 myoblasts, mouse C2C12 myoblasts, and mouse skeletal muscle satellite cells). Dietary relevant concentration of Nar delays the appearance of skeletal muscle differentiation markers (i.e., GLUT4 translocation, myogenin, and both fetal and slow MHC isoforms) and impairs E2 effects specifically hampering ERa ability to activate AKT. Intriguingly, Nar effects are specific for E2-initiating signals because IGF-Iinduced AKT activation, and myoblast differentiation markers were not affected by Nar treatment. Only 7 days after Nar stimulation, early myoblast differentiation markers (i.e., myogenin, and fetal MHC) start to be accumulated in myoblasts. On the other hand, Nar stimulation activates, via ERb, the phosphorylation of p38/MAPK involved in reducing the reactive oxygen species formation in skeletal muscle cells. As a whole, data reported here strongly sustain that although Nar action mechanisms include the impairment of ERa signals which drive muscle cells to differentiation, the effects triggered by Nar in the presence of ERb could balance this negative effect avoiding the toxic effects produced by oxidative stress.

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“…Current data show that all cancer types are in some way related with the level of estrogen, estrogen receptors and aromatase or their polymorphisms [11][12][13][14]. Generally estrogen receptor (ER) alpha promotes proliferation, while ER beta supresses it but this is not the rule for all tissues; moreover, the ER status varies between neoplastic tissues.…”

Section: Introductionmentioning

confidence: 99%

Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

Fučić¹,

Mantovani²

2015

TOBIOTJ

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Susceptibility to environmental stressors, same as cancer incidence is both age and gender related. Understanding the complexity of responses to living environment has been impaireddue to research based on reductionisms and lack of methods, models and sophisticated softwares which enable analysis of complex pathways which may be disturbed by xenobotics. Impact of estrogen on development, maturation and homeostasis of organism in both genders is now well recognised and environmental investigations are currently making major efforts to understand how xenoestrogens affect organisms at very low doses.Additionally, it is of great interest to learn possible synergistic or antagonistic effects of xenoestrogen mixtures on adult organism and during development. The aim of this paper is to review the findings on the association between cancer risk and the endocrine disrupters which directly or indirectly mimic estrogen action.

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The different roles of ER subtypes in cancer biology and therapy

Cited by 574 publications

References 164 publications

Induction of estrogen receptor α-36 expression by bone morphogenetic protein 2 in breast cancer cell lines

Induction of estrogen receptor α-36 expression by bone morphogenetic protein 2 in breast cancer cell lines

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

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