Inhibitory effect of apatinib on HCT-116 cells and its mechanism
YIN Liang
WANG Jin
HUANG Fengchang
ZHANG Yunfei
XU Ning
WEN Zhengqi
LI Wenliang
DONG Jian
Abstract：Objective To investigate the inhibitory effects of apatinib on colorectal carcinoma HCT-116 cells in vitro and the signaling pathways involved.Methods The cytotoxicity of different concentrations (0,0.5,1,1.5,and 2 μmol/L) of apatinib in HCT-116 cells was assessed by MTT assay,using capecitabine as the positive control.The apoptosis rate of apatinib-treated HCT-116 cells was detected using flow cytometry,and the expressions of Bcl-2,Bax,and caspase-3 were determined with quantitative real-time PCR and Western blotting.The effect of apatinib on the expressions of Akt,pAkt,Erkl/2 and pErk1/2 in HCT-116 cells was evaluated using Western blotting.Results Apatinib significantly inhibited the proliferation of HCT-116 cells in a concentration-dependent manner with an IC50 value of 1.335 μmol/L.Flow cytometric analysis showed that apatinib significantly increased the apoptotic rate of HCT-116 cells dose-dependently.Apatinib induced the expression of the pro-apoptotic genes Bax and caspase-3 at both the mRNA and protein levels while inhibited the expression of the antiapoptotic gene Bcl-2.The expressions of p-Akt and p-Erkl/2 were decreased in HCT-116 cells after apatinib treatment,but the total protein levels did not undergo obvious changes.Conclusion Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erkl/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.
Keywords：apatinibHCT-116 cellsapoptosisMAPK/Erk signaling pathwayPI3K/Akt signaling pathway
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：6( 367-372 )