Home > Browse Issues > Vol.37 No.12
Influence of Gefitinib on Proliferation and Apoptosis of HepG2 Cells with ANXA7 Knockdown
Jiao Haitao1, Wang Aimin2, Tian Huanna1, Wang Xiaojie1, Liang Xiujun1, Li Xin1*
1Chengde Medical University, Chengde 067000, China; 2Chengde Central Hospital, Chengde 067000, China
Abstract: The paper aimed at investigating the influences of Gefitinib on the proliferation and apoptosis of HepG2 cells with annexin A7 (ANXA7) knockdown in order to developing a potential therapy for hepatocellar carcinoma. The human hepatoblastoma cell line HepG2 cells were incubated for three days with Gefitinib at different concentrations ranging from 0.1 to 50, and then studied by MTT to measure 50% inhibitory concentration (IC50) of Gefitinib, the IC50 was 5 μmol/L. The cells were divided into A7si combine Gefitinib group, Gefitinib group, A7si group, negative control group and blank control group. RNA interference technology was used to transfect the siRNA targeted ANXA7, scrambled siRNA into HepG2 cells with lipofectine 2000. After 72 hours, the suppression of ANXA7 on protein level was assured by Western blot. The inhibitory rate was tested using MTT assay and the apoptosis ratio was detected by flow cytometry. The results showed that HepG2 cells proliferation was significantly suppressed with Gefitinib concentration increasing in a does-dependent manner. The suppression of ANXA7 on protein level was assured by Western blot. It also showed by MTT assay and Flow cytometry that the inhibition rate and apoptotic rate of the HepG2 cells in the A7si combine Gefitinib group, Gefitinib group and A7si group, were much higher than that in the negative control group and the blank control group (P<0.05). When compared A7si combine Gefitinib group with Gefitinib group and A7si group respectively, the A7si combine Gefitinib group had the greatest effect of proliferation inhibition and apoptosis promotion. Taken together, our results suggested that Gefitinib and ANXA7 knockdown can synergistically inhibit HepG2 cell proliferation, and promote cell apoptosis which might be a potential method for clinic treatment.