Steroids and the Endometrium

Oehler, Martin K.; Rees, Margaret; Bicknell, Roy

doi:10.2174/0929867003374958

Cited by 34 publications

(10 citation statements)

References 70 publications

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“…They are liganddependent transcription factors that, on activation, bind to distinct DNA target sites to modulate the expression of specific genes. In addition to this direct activation of target genes, indirect mechanisms acting through contacts with DNA-bound transcription factors such as AP-1 or NF-κB have been described (Oehler et al 2000).…”

Section: Steroid Receptor Genesmentioning

confidence: 99%

Endometrial cancer

et al. 2005

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Endometrial cancer is the most common gynaecological malignancy in the developed world. The majority of cases can be divided into two broad categories based on clinico-pathological and molecular characteristics; Type I oestrogen-dependent with endometrioid morphology and Type II non-oestrogen-dependent with serous papillary or clear cell morphology. As has been described for other malignancies, such as colorectal carcinoma, the transition from normal endometrium to carcinoma is thought to involve a stepwise accumulation of alterations in cellular regulatory pathways leading to dysfunctional cell growth. This article reviews the current knowledge of the molecular changes commonly associated with endometrial cancer and presents possible progression models.

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Section: Steroid Receptor Genesmentioning

confidence: 99%

Endometrial cancer

et al. 2005

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“…There are two distinct ERs that are activated by the binding of estradiol: ERa and ERb. Also, the progesterone receptors (PRs) exist in two isoforms that are the products of the same gene, where PRA lacks 164 amino acids from the N-terminal end of PRB [15].…”

Section: Introductionmentioning

confidence: 99%

Expression analysis of the genes involved in estradiol and progesterone action in human ovarian endometriosis

Šmuc

Šinkovec

et al. 2007

Gynecological Endocrinology

112

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Endometriosis is defined as the presence of endometrial glands and stroma within extrauterine sites, and it is well known that endometriosis is an estrogen-dependent disease. The defective formation and metabolism of steroid hormones is responsible for the promotion and development of endometriosis. In the present study we examined the mRNA levels of six enzymes that are involved in the metabolism of estrogen and progesterone--aromatase, 17beta-hydroxysteroid dehydrogenase (17beta-HSD) types 1, 2 and 7, sulfatase and sulfotransferase--and of the steroid receptors--estrogen receptors alpha and beta (ERalpha, ERbeta) and progesterone receptors A and B (PRAB)--implicated in human ovarian endometriosis. We analyzed 16 samples of ovarian endometriosis and 9 of normal endometrium. The real-time polymerase chain reaction analyses revealed that six of the nine genes investigated are differentially regulated. Aromatase, 17beta-HSD types 1 and 7, sulfatase and ERbeta were statistically significantly upregulated, while ERalpha was significantly downregulated, in the endometriosis group compared with the control group. There were no significant differences in 17beta-HSD type 2, sulfotransferase and PRAB gene expression. Our results indicate that, in addition to the previously reported upregulation of aromatase, upregulation of 17beta-HSD types 1 and 7 and sulfatase can also increase the local estradiol concentration. This could thus be responsible for the estrogen-dependent growth of endometriotic tissue. Surprisingly ERalpha was downregulated.

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“…Conversely, the role of progesterone in vascular wall cells has been extensively described [Oehler et al, 2000;Dabrosin, 2005b]. Angiogenesis is a complex multistep process that comprises endothelial cell, as well as support cell proliferation, migration, and invasion [Soares et al, 2003a;Costa et al, 2004].…”

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confidence: 99%

Elucidating progesterone effects in breast cancer: Cross talk with PDGF signaling pathway in smooth muscle cell

Soares

Guerreiro

Botelho

2006

J of Cellular Biochemistry

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Several studies indicate that progesterone exerts relevant effects in breast tissue. However, the exact role of this steroid in breast cancer development and progression has not been elucidated. Here, we show that platelet-derived growth factor (PDGF)-A is one of the progesterone target genes on breast cancer MCF7 and T47D cells. A paracrine role for PDGF-A was investigated, since its receptor expression was down-regulated from breast cancer cells. Progesterone increased PDGF-A protein release as evaluated by Western blotting and ELISA. Medium from Progesterone-treated MCF7 cells resulted in phosphorylation of smooth muscle cells PDGF receptor a. This effect was not observed after treatment with PDGF inhibitor. MCF7 cells-secreted PDGF-A was able to increase smooth muscle cell viability and proliferation and decrease apoptosis, effects that were prevented by the use of a PDGF-A neutralizing antibody. Notably, cell invasion was not influenced by PDGF-A secreted by MCF7 cells. Our results elucidated for the first time the cross talk between progesterone and PDGF signaling pathway. The fact that MCF7-secreted PDGF elicited crucial roles in vascular wall smooth muscle cells, suggested a paracrine pathway for progesterone. Targeting these progesterone-induced processes may provide novel therapeutic strategies for hormone-dependent human breast cancer.

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Steroids and the Endometrium

Cited by 34 publications

References 70 publications

Endometrial cancer

Endometrial cancer

Expression analysis of the genes involved in estradiol and progesterone action in human ovarian endometriosis

Elucidating progesterone effects in breast cancer: Cross talk with PDGF signaling pathway in smooth muscle cell

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