Cadherin-11 is a hormonally regulated cellular marker of decidualization in human endometrial stromal cells

Chen, George T.C.; Getsios, Spiro; MacCalman, Colin D.

doi:10.1002/(sici)1098-2795(199902)52:2<158::aid-mrd6>3.0.co;2-3

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…Moreover, forcedexpression of cadherin-11 has been shown to induce the up-regulation of proinvasive genes, including N-cadherin and TWIST (45). In addition to being expressed by EVT cells, cadherin-11 is expressed in syncytiotrophoblasts and decidualizing stromal cells (46,47). A role in syncytialization has been suggested since antisense oligonucleotides targeting cadherin-11 can block the fusion and terminal differentiation of primary villous cytotrophoblasts (21).…”

Section: Discussionmentioning

confidence: 99%

“…A role in syncytialization has been suggested since antisense oligonucleotides targeting cadherin-11 can block the fusion and terminal differentiation of primary villous cytotrophoblasts (21). Cadherin-11 may also be important for interactions between trophoblasts and endometrial epithelial or decidualized endometrial stromal cells (20,47). Future studies investigating additional functional roles for cadherin-11 in placental biology will be of interest.…”

Section: Discussionmentioning

confidence: 99%

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AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Peng

Zhu

et al. 2015

Endocrinology

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GnRH is expressed in first-trimester human placenta and increases cell invasion in extravillous cytotrophoblasts (EVTs). Invasive phenotypes have been reported to be regulated by transcription factor activator protein 1 (AP-1) and mesenchymal cadherin-11. The aim of our study was to investigate the roles of AP-1 components (c-FOS/c-JUN) and cadherin-11 in GnRH-induced cell invasion in human EVT cells. Phosphorylated c-FOS and phosphorylated c-JUN were detected in the cell column regions of human first-trimester placental villi by immunohistochemistry. GnRH treatment increased c-FOS, c-JUN, and cadherin-11 mRNA and protein levels in immortalized EVT (HTR-8/SVneo) cells. Moreover, GnRH treatment induced c-FOS and c-JUN protein phosphorylation and nuclear accumulation. Pretreatment with antide, a GnRH antagonist, attenuated GnRH-induced cadherin-11 expression. Importantly, basal and GnRH-induced cadherin-11 expression and cell invasion were reduced by small interfering RNA-mediated knockdown of c-FOS, c-JUN, and cadherin-11 in HTR-8/SVneo cells. Our results suggest that GnRH induces the expression and phosphorylation of the AP-1 transcription factors c-FOS and c-JUN in trophoblast cells, which contributes to GnRH-induced elevation of cadherin-11 expression and cell invasion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Peng

Zhu

et al. 2015

Endocrinology

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“…Although little work has been done to elucidate its role, Cad-11 may be important in promoting adhesion of trophoblast to maternal stromal cells, where it is upregulated during decidualization [60]. Similarly, expression of dysadherin, a cell 215 surface glycoprotein thought to reduce cell-cell adhesion and increase motility, is increased in CTB developing into columns [61,62].…”

Section: Ve-cadherin (Ve-cad) a Marker Of The Endothelial Cell Lineamentioning

confidence: 99%

Adhesion Molecules in Human Trophoblast – A Review. II. Extravillous Trophoblast

2009

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“…They found that progesterone, but not E2 or dihydroestosterone, was capable of regulating Cad-11 expression. However, E2 was capable of potentiating the stimulating effects of progesterone in a dose-dependent manner [172,173], and that the antiestrogen, ICI182780, was capable of reducing Cad-11 expression in these cells, suggesting the requirement of estrogens and ERs in mediating these effects [174]. Gorodeski [175] studied the effects of estrogens and aging on paracellular permeability of human vaginal-cervical epithelia by determining the transepithelial electrical conductance (TEC) across cultures of normal human ectocervical epithelial cells on filters.…”

Section: Estrogens and Ers Are Involved In The Regulation Of Tight Anmentioning

confidence: 99%

“…Aberrant (usually reduced or loss) expression of various components of TJs and AJs has been frequently observed in breast cancer cells [70,87,98]. E2 suppresses, directly or indirectly, the expression of several groups of components of TJs and AJs [172][173][174]176,195,196]. These effects could be particularly important in human breast cells, since they are exposed to relatively high E 2 levels due to the in situ E 2 synthesis by local aromatase activity [22][23][24]26].…”

Section: A Novel Concept and A New Paradigmmentioning

confidence: 99%

Sodium/potasium ATPase (Na+, K+-ATPase) and ouabain/related cardiac glycosides: a new paradigm for development of anti- breast cancer drugs?

Chen

Contreras

Wang

et al. 2005

Breast Cancer Res Treat

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Prolonged exposure to 17beta-estradiol (E2) is a key etiological factor for human breast cancer. The biological effects and carcinogenic effects of E2 are mediated via estrogen receptors (ERs), ERalpha and ERbeta. Anti-estrogens, e.g. tamoxifen, and aromatase inhibitors have been used to treat ER-positive breast cancer. While anti-estrogen therapy is initially successful, a major problem is that most tumors develop resistance and the disease ultimately progresses, pointing to the need of developing alternative drugs targeting to other critical targets in breast cancer cells. We have identified that Na+, K+-ATPase, a plasma membrane ion pump, has unique/valuable properties that could be used as a potentially important target for breast cancer treatment: (a) it is a key player of cell adhesion and is involved in cancer progression; (b) it serves as a versatile signal transducer and is a target for a number of hormones including estrogens and (d) its aberrant expression and activity are implicated in the development and progression of breast cancer. There are several lines of evidence indicating that ouabain and related digitalis (the potent inhibitors of Na+, K+-ATPase) possess potent anti-breast cancer activity. While it is not clear how the suggested anti-cancer activity of these drugs work, several observations point to ouabain and digitalis as being potential ER antagonists. We critically reviewed many lines of evidence and postulated a novel concept that Na+, K+-ATPase in combination with ERs could be important targets of anti-breast cancer drugs. Modulators, e.g. ouabain and related digitalis could be useful to develop valuable anti-breast cancer drugs as both Na+, K+-ATPase inhibitors and ER antagonists.

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Cadherin-11 is a hormonally regulated cellular marker of decidualization in human endometrial stromal cells

Cited by 22 publications

References 29 publications

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Adhesion Molecules in Human Trophoblast – A Review. II. Extravillous Trophoblast

Sodium/potasium ATPase (Na+, K+-ATPase) and ouabain/related cardiac glycosides: a new paradigm for development of anti- breast cancer drugs?

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