Estrogen Receptor Beta Displays Cell Cycle-Dependent Expression and Regulates the G1 Phase through a Non-Genomic Mechanism in Prostate Carcinoma Cells

摘要: Background: It is well known that estrogens regulate cell cycle progression, but the specific contributions and mecha- nisms of action estrogen receptor beta (ERβ) remain elusive. Methods: We have analyzed levels ERβ 1a nd ERβ2 throughout cycle, as mechanisms consequences over-expression ERβ1 in human prostate cancer LNCaP line. Results :B oth mRNA protein expression increased from G1 to S phase decreased before entering G2/M phase, whereas during phase. was detected both nuclear non-nuclear fractions, found exclusively nucleus. Regarding action, endogenous able activate transcription via ERE a ligand-dependent manner, no changes AP1 NFκB transactivation were observed after exposure estradiol or inhibitor ICI 182,780. Over-expression either wild type 1o r mutated DNA-binding domain caused an arrest early G1. This accompanied by interaction over-expressed with c-Jun N-terminal kinase 1 (JNK1) decrease phosphorylation cyclin D1 expression. The administration impeded JNK1-ERβ1 interaction, allowed cells progress late G1, where they became arrested. Conclusions: Our results demonstrate that, cells, isoforms are differentially expressed regulates non-genomic mechanism.