Abstract
We report in this study that proliferation inhibition of SCC13 cells by calcipotriol was possibly mediated by its inhibitory effect on autocrine activation of EGF receptor. Based on MTT assay, PCNA staining, DAPI staining, and involucrin immunocytochemical staining, we showed that calcipotriol inhibited cell growth and stimulated differentiation but did not induce apoptosis. Western blot analysis of concanavalin-A-bound fraction demonstrated that calcipotriol specifically dephosphorylated 170- and 66-kDa polypeptides from 8 h posttreatment and complete dephosphorylation was observed at 12 h posttreatment. The 170- and 66-kDa polypeptides were confirmed as EGF receptor and Shc, respectively. Calcipotriol-mediated EGF receptor dephosphorylation required the presence of extracellular calcium. Similar kinetics of the dephosphorylation was also observed in HaCaT cells cultured in medium of high calcium concentration. By BrdU labeling, we also showed calcium dependency of calcipotriol for the inhibition of cell proliferation. Therefore, EGF receptor deactivation by calcipotriol might be a mechanism of action for the inhibition of cell proliferation and the stimulation of differentiation in SCC13 cell and HaCaT cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
