Estrogen Enhances the Cell Viability and Motility of Breast Cancer Cells through the ERα-ΔNp63-Integrin β4 Signaling Pathway.

摘要: Estrogen induces ERα-positive breast cancer aggressiveness via the promotion of cell proliferation and survival, epithelial-mesenchymal transition, stem-like properties. Integrin β4 signaling has been implicated in estrogen/ERα-induced tumorigenicity anti-apoptosis; however, this cascade poorly understood. ΔNp63, an N-terminally truncated isoform p63 transcription factor, functions as a factor integrinβ4 therefore regulates cellular adhesion survival. Therefore, aim present study was to investigate estrogen-induced interaction between ERα, ΔNp63 integrin cells. In MCF-7 cells, estrogen activated ERα transcription, which induced expression. And subsequently expression, resulted AKT phosphorylation enhanced viability motility. Conversely, there no inductive effect on ΔNp63-integrinβ4-AKT or motility ERα-negative MDA-MB-231 knockdown abolishes these effects reduces Nevertheless, also inhibited migration cells through reducing expression phosphorylation. conclusion, enhances activating ERα-ΔNp63-integrin pathway induce phosphorylated activation. Those findings should be useful elucidate crosstalk estrogen/ER provide novel insights into progression.