Both nongenomic and genomic effects are involved in estradiol's enhancing the phenotype of smooth muscle cells in cultured prostate stromal cells

Abstract

Estrogen could promote the expression of TGF-beta1 in PRSCs through nongenomic activation of MAPK pathway, and in turn enhance the SMC phenotype. Besides for this nongenomic effect, estrogen can also enhance the SMC phenotype through classical genomic action.

Epithelial-to-mesenchymal transition and estrogen receptor α mediated epithelial dedifferentiation mark the development of benign prostatic hyperplasia

“…The observed tissue alterations are triggered by enhanced estrogenic activity and can be prevented by raloxifene in the animal model. Estrogens elicit a proliferative response in the prostate and were shown to stimulate epithelial as well as stromal cells , however, as shown in a transgenic mouse model by selective ERα knockout either in the stroma or the epithelium, epithelial ERα is required for induction of BPH . On the basis of our data, we suggest that EMT elicited in the prostate epithelium is the initial trigger.…”

“…However, an increased percentage of ERα positive epithelial cells are observed in BPH tissue , which are pre‐dominantly of a basal cell type and estrogens were shown to promote basal cell proliferation via epithelial ERα . With regard to the prostatic stroma there is a bulk of evidence from human and animal models that estrogens stimulate proliferation and induce differentiation towards a smooth muscle cell phenotype in stromal cells of the prostate . Despite this stromal response selective ERα knockout in mice identified the epithelial ERα as a crucial requirement for an estrogen‐triggered proliferative response .…”

Prohibitin-2 negatively regulates AKT2 expression to promote prostate cancer cell migration

“…Total RNA was extracted from PC3 and DU145 cells using TRIzol reagent (Invitrogen; Thermo Fisher Scientific, Inc.). RT was performed for 2 h at 37˚C as described previously (32). RT-PCR reagents were purchased from Invitrogen; Thermo Fisher Scientific, Inc. (cat.…”

Estradiol promotes epithelial‐to‐mesenchymal transition in human benign prostatic epithelial cells

“…It has been well established that androgen and estrogen synergistically regulate the growth and development of normal prostate as well as drive BPH pathogenesis . Estrogen regulates the phenotype of prostatic smooth muscle cells through both nongenomic and genomic effects and enhances the proliferation of stromal cells by activating the ERK signaling pathway . Our group has also established a stromal BPH rat model induced by E2 and testosterone (T) treatment via gavage according to a defined E2/T ratio .…”