Effect of FABP5 gene silencing on the proliferation, apoptosis and invasion of human gastric SGC-7901 cancer cells

FABP5基因沉默对人胃癌SGC-7901细胞增殖、凋亡及侵袭的影响

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作者:Guanjie Zhao, Minfei Wu, Xiaofeng Wang, Zhenwu Du, Guizhen Zhang

Abstract

The aim of the present study was to examine the effect of fatty acid binding protein-5 (FABP-5) gene on the proliferation, apoptosis and invasion of human gastric cancer SGC-7901 cells. The viability, apoptosis and cell invasion of SGC-7901 cells before and after FABP5 knockdown were taken as the study objects, design and synthesis of siRNA interference sequence were conducted according to FABP-5 mRNA coding sequences, and SGC-7901 cells were transiently transfected. The human gastric cancer SGC-7901 cells were divided into three groups: FABP-5 siRNA group, negative control group and blank control group. FABP-5 gene mRNA and protein expression levels were detected by RT-PCR and western blot analysis. The CCK-8 assay was used to detect in vitro cell proliferation, flow cytometry (FCM) was used to detect changes in cell cycle and apoptosis in each group, TUNEL staining was used to detect apoptosis in each group, and the cell invasion chamber assay was used to detect cell invasiveness in each group. Each test was repeated three times. The results of the RT-PCR and western blot analysis showed that, expression of FABP-5 mRNA and protein in the FABP-5 siRNA group was significantly decreased compared with the negative and blank control groups. The cell growth rate in the FABP-5 siRNA group was significantly retarded, cell cycle was arrested in G0/G1 phase, the number of cells in S phase was reduced, and compared with the negative and blank control groups, the apoptotic rate in the FABP-5 siRNA group was significantly increased (P<0.01), while proliferation and invasiveness were significantly decreased (P<0.05). In conclusion, specific FABP-5 gene silencing may reduce the invasiveness of gastric cancer cells, inhibit cell proliferation, and arrest cell cycle in G0/G1 phase, resulting in a significant increase in apoptosis.

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