Effect of Abl-interacting protein 1 overexpression upon human gastric cancer cell proliferation in vitro

Abstract

To investigate the expression of Abl-interacting protein 1 (ABI1) in normal gastric mucosal cell line GES-1 and gastric cancer cell line AGS, and the effects of ABI1 gene overexpression upon the proliferation of human gastric cancer cell AGS in vitro. Firstly the ABI1 expression in GES-1 and AGS cells were identified by immunohistochemistry, immunofluorescence, RT-PCR, real-time PCR and Western blot. Secondly human gastric cancer cell line AGS was cultured and transfected with recombinant MSCV-GFP-ABI1 plasmid or blank plasmid MSCV-GPF. Real-time PCR and Western blot were used to detect the mRNA and protein expression of ABI1. And lastly the cell proliferation was detected by CCK-8 assay. ABI1 was expressed both in normal gastric mucosal cell line GES-1 and in gastric cancer cell line AGS. Compared to GES-1 cells, the ABI1 expression in AGS cells was lowered significantly. There were no significant differences in the ABI1 mRNA and protein expression between the AGS and AGS-MSCV-GFP groups. Compared to those of the AGS group, the ABI1 mRNA expression levels of the AGS-MSCV-GFP-ABI1 group increased by 1.87 times (P = 0.002). The protein expression levels of the AGS-MSCV-GFP-ABI1 group were remarkably higher than those of the AGS and AGS-MSCV-GFP groups (P = 0.002). CCK-8 assay showed that there were no significant differences in the proliferation rates at different time points between the AGS and AGS-MSCV-GFP groups. However, the proliferation rates at the time points of 24, 48, 72 and 96 hours of the AGS-MSCV-GFP-ABI1 were 1.46 +/- 0.31, 4.75 +/- 0.12, 6.62 +/- 0.32 and 8.96 +/- 0.27 respectively. And they were significantly lower than the proliferation rates of the AGS and AGS-MSCV-GFP groups (P < 0.01). ABI1 gene is down-regulated in gastric cancer cells. The ABI1 overexpression effectively inhibits the proliferation in human gastric cancer cell lines. It suggests that ABI1 may be involved in gastric cancer pathogenesis by regulating the proliferation of gastric carcinomas cells.