作者: Kuan-Hui Ethan Chen , Karissa Bustamante , Vi Nguyen , Ameae M. Walker
DOI: 10.18632/ONCOTARGET.16755
关键词: Endocrinology 、 MAPK/ERK pathway 、 Internal medicine 、 PI3K/AKT/mTOR pathway 、 Cell growth 、 Prolactin cell 、 Signal transduction 、 Cancer research 、 Cancer cell 、 Protein kinase B 、 Prolactin 、 Biology
摘要: Prolactin promotes a variety of cancers by an array different mechanisms. Here, we have investigated prolactin's inhibitory effect on expression the cell cycle-regulating protein, p21. Using miRNA array, identified number miRNAs upregulated prolactin treatment, but one in particular that was strongly induced and predicted to bind 3'UTR p21 mRNA, miR-106b. By creating mRNA 3'UTR-luciferase construct, demonstrated degradation construct response human breast, prostate ovarian cancer lines. Increased miR-106b replicated, anti-miR-106b counteracted, effects levels, proliferation breast (T47D) (PC3) cells. also stimulated migration very epithelioid T47D line. contrast, dramatically decreased mesenchymal markers, SNAIL-2, TWIST-2, VIMENTIN, FIBRONECTIN. signaling pathway inhibitors induction determined be mediated through MAPK/ERK PI3K/Akt pathways not Jak2/Stat5 both PC3 activation activates ERα absence ligand. 17β-estradiol promoted lines pre-incubation estrogen antagonist, Fulvestrant, blocked ability induce construct-degrading activity. Together, these data support convergence miR-106b-elevating at ERα.