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Curcumol induces cell cycle arrest and apoptosis by inhibiting IGF‐1R/PI3K/Akt signaling pathway in human nasopharyngeal carcinoma CNE‐2 cells
Author(s) -
Li Xumei,
Liu Haowei,
Wang Juan,
Qin Jianli,
Bai Zhun,
Chi Bixia,
Yan Wei,
Chen Xu
Publication year - 2018
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6158
Subject(s) - nasopharyngeal carcinoma , pi3k/akt/mtor pathway , protein kinase b , apoptosis , cell cycle checkpoint , cell cycle , cancer research , signal transduction , chemistry , carcinogenesis , cell growth , microbiology and biotechnology , biology , medicine , biochemistry , radiation therapy , gene
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.