Abstract
Curcumol has been proved to possess antitumor effects in vivo and in vitro in several cancers. Previously, we have found that curcumol induced apoptosis in CNE-2 cells, but its underlying mechanism has not yet been studied well. Recently, our team clarified that curcumol inhibited colorectal cancer cells' growth partially through insulin-like growth factor 1 receptor (IGF-1R) pathway. Given the key importance of IGF-1R pathway in tumorigenesis, we want to explore whether curcumol effects on nasopharyngeal carcinoma (NPC) cells relates to IGF-1R and its downstream pathway inactivation. In this study, we found that curcumol inhibited IGF-1R and p-Akt expression in a dose- and time-dependent way. In addition, it also regulated their downstream GSK-3β's activity in CNE-2 cells, which further triggering alterations in the expression of cycle- and apoptosis-related molecules, and then leading to G0/G1-phase arrest and apoptosis. Moreover, curcumol's effect on CNE-2 cells was partly eliminated by IGF-1R's agonist IGF-1. In conclusion, our findings indicated that the inhibitory effect of curcumol on proliferation of NPC cells is related to the inhibition of IGF-1R and its downstream PI3K/Akt/GSK-3β pathway.
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