Estrogen regulation of cell cycle progression in breast cancer cells

Prall, Owen W.J.; Rogan, Eileen M.; Sutherland, Robert L.

doi:10.1016/s0960-0760(98)00021-1

Cited by 147 publications

(110 citation statements)

References 36 publications

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“…In addition, the repeated breeding protocol not only activates the MMTV promoter, but also generates high levels of pregnancyrelated hormones that may provide proliferative stimuli for the growth of epithelial cells. Estrogen is a major candidate for the hormones produced during pregnancy given a role of this factor in promoting breast cancer formation (Colditz, 1998;Prall et al, 1998;Gadducci et al, 2005). Zhang et al (2004) also reported that overexpression of Aurora-A in mammary epithelium induced an accumulation of p53 and p53-dependent apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation

et al. 2006

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“…For example, ER interferes with AP1-directed gene activity [20][21][22] through a protein-protein interaction with c-Jun. In cell cultures, genes such as cyclin D1 are stimulated by estrogens through an AP-1 pathway and repressed by tamoxifen [67]. By contrast, the non-genomic effects of estrogens on signal transduction do not appear implicated in their mitogenic action, since all key events in cell cycle stimulation can occur in the presence of a MAP kinase-activating inhibitor [68].…”

Section: Involved Mechanisms?mentioning

confidence: 99%

“…The genes responsible for the mitogenic effect of estrogens have not been definitively determined but they probably include secreted growth factors [65], growth factor receptors [69,70], proteases such as cathepsin D [71] and cyclin/cdk factors [67]. The implication of molecules interfering with the cytoskeleton, such as E-cadherin, a mediator of cell-cell interactions,as been also suggested [72].…”

Section: Involved Mechanisms?mentioning

confidence: 99%

Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

Platet

Cathiard

Gleizes

et al. 2004

Critical Reviews in Oncology/Hematology

319

236

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Estrogens play an important role in regulating the growth and differentiation of normal, premalignant and malignant cell types, especially breast epithelial cells, through interaction with two nuclear estrogen receptors (ER and ERIn this review, we present a brief overview of the actions of estrogens in the different steps of breast carcinogenesis, including cancer progression to metastasis, and of their clinical consequences in the prevention, prognosis and treatment of the disease. The requirement of estrogen receptors, mainly of the alpha subtype, in normal mammary gland differentiation and growth has been evidenced by estrogen receptor deficiency in animals. The promotion of breast cancer carcinogenesis by prolonged exposure to estrogens is well-documented and this has logically led to the use of antiestrogens as potentially chemopreventive agents. In breast cancer progression, however, the exact roles of estrogen receptors have been less well established but they may possibly be dual. Estrogens are mitogenic in ER-positive cells and antiestrogens are an efficient adjuvant therapy for these tumors. On the other hand, the fact that estrogens and their receptors protect against cancer cell invasiveness through distinct mechanisms in experimental models may explain why the presence of ER is associated with well-differentiated and less invasive tumors.2

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“…It was reported recently that BRCA1 inhibits estrogen biosynthesis through modulating aromatase expression in ovarian granulosa cells (Hu et al, 2005). Data obtained from numerous in vivo observations indicated that estrogen could promote breast cancer formation and, conversely, the administration of tamoxifen, which blocks ERa signaling reduced cancer risk (Prall et al, 1998;Calderon-Margalit and Paltiel, 2004;Gadducci et al, 2005). Moreover, oophorectomy in human BRCA1 mutation carriers and in mouse mutants carrying mammary-specific BRCA1 mutations also significantly reduced the frequency of breast/mammary cancer formation (Kauff et al, 2002;Bachelier et al, 2005).…”

Section: Introductionmentioning

confidence: 97%

A role of estrogen/ERα signaling in BRCA1-associated tissue-specific tumor formation

Xiao

et al. 2007

Oncogene

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Estrogen and its receptor alpha (ERa) have been implicated in the tissue-specific tumorigenesis associated with BRCA1 mutations. However, the majority of breast cancers developed in human BRCA1 mutation carriers are ERa-negative, challenging the link between BRCA1 and estrogen/ERa in breast cancer formation. Using a mouse model lacking the full-length form of BRCA1, here we show that ERa is highly expressed in the premalignant mammary gland and initiation stages of tumorigenesis, although its expression is gradually diminished during mammary tumor progression. We demonstrate that the absence of full-length BRCA1 increases sensitivity of cells to estrogen-induced extracellular signal-regulated kinase 1/2 phosphorylation and cyclin D1 expression. The absence of BRCA1 turns the proliferation of ERa-positive cells from a paracrine fashion to an autocrine or endocrine fashion. Consequently, BRCA1-mutant cells are sensitized to estrogen-induced cell proliferation in vitro and mammary tumorigenesis in vivo. These findings illustrate a molecular mechanism for estrogen/ERa signals in BRCA1-associated tissue-specific tumor formation, and identify several key elements in the estrogen/ERasignaling cascade that can serve as potential therapeutic targets for BRCA1-associated tumorigenesis.

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Estrogen regulation of cell cycle progression in breast cancer cells

Cited by 147 publications

References 36 publications

Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation

Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation

Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

A role of estrogen/ERα signaling in BRCA1-associated tissue-specific tumor formation

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