Differential engagement of ORAI1 and TRPC1 in the induction of vimentin expression by different stimuli.

摘要: The Ca2+ signal is essential in both hypoxia- and epidermal growth factor (EGF)-mediated epithelial to mesenchymal transition (EMT) MDA-MB-468 breast cancer cells. This finding suggests that Ca2+-permeable ion channels participate the induction of expression some markers such as vimentin. However, involved vimentin have not been fully characterized. work sought define how differential modulation calcium effects influx pathways involved. We identified intracellular chelator EGTA-AM, cytochalasin D (a modulator cytoskeletal dynamics cell morphology), sarco/endoplasmic reticulum ATPase inhibitor thapsigargin are all inducers EGTA-AM- thapsigargin-mediated cells involves store-operated entry, evidenced by sensitivity silencing molecular components this pathway, STIM1 ORAI1. In stark contrast, D-mediated was insensitive ORAI1, despite its canonical activator endoplasmic sensor STIM1. Cytochalasin was, however, sensitive another reported target, TRPC1. Subsequent studies EGTA-AM-induced also partially a TRPC1-dependent pathway. These complex interplay between model specific complexity engagement different regulate opportunities but potential challenges targeting signaling block EMT Our findings further highlight need identify indispensable can via stimuli.