RASSF6 plays a role in suppressing cancer and improving the sensitivity of oxaliplatin in gastric cancer cells / 西安交通大学学报(医学版)

ABSTRACT

【Objective】 To investigate the effects of RASSF6 gene on gastric cancer cells’ proliferation， autophagy， apoptosis， and sensitivity to oxaliplatin chemotherapy. 【Methods】 Gastric cancer BGC823 cells were cultured in vitro and divided into experimental control group （control group）， RASSF6 overexpression group （Oe group）， RASSF6 interference group， and lentivirus control group according to the expression effect of lentivirus gene. The changes in cell proliferation， cell cycle distribution， cell migration， autophagy， apoptosis and sensitivity to oxaliplatin in each group were detected， and the number of autophagy bodies in each group was detected by electron microscopy. Real-time PCR （qRT-PCR） and Western blotting were used to detect the expression levels of apoptosis- and autophagy-related genes in each group. 【Results】 Studies on the biological behavior of gastric cancer BGC823 cells induced by RASSF6 gene expression showed that compared with the control group， the percentage of G0/G1 phase cells in the Oe group increased， while the percentage of G2 and S phase cells decreased， with statistical significance （P<0.05）. The apoptosis rate was significantly increased （P<0.05）. The cell scratch assay showed that the scratch healing rate was significantly decreased （P<0.05）. Studies on the sensitivity of RASSF6 gene expression to oxaliplatin showed that compared with the drug group （L-OHP group）， the apoptosis rate of Oe+L-OHP group was increased significantly （P<0.05）. In the Oe+L-OHP group， the expression of anti-apoptotic protein Bcl-2 decreased， the expressions of Bax and Caspase-3 were increased； the expression of autophagosomes was increased； the expressions of Beclin-1 and P62 and the ratio of LC3-Ⅱ/LC3 were all increased （P<0.05）. 【Conclusion】 The RASSF6 gene plays a role in suppressing gastric cancer cell BGC823， which can increase the sensitivity to oxaliplatin chemotherapy by promoting apoptosis and autophagy.