Effect Of RACK1 On Biological Behavior Of Lung Adenocarcinoma Cell Line A549 And VEGF, Bcl-2, CyclinD1 Expression

Objective:To investigate the effect of silencing RACK1(receptor for activated C kinase 1) on biological behavior of lung adenocarcinoma cell line A549 and explore its effect on VEGF, Bcl-2, Cyclin D1 expression. Methods:The sh RNA targeting RACK1 gene and empty plasmid were transfected into A549 cells by lipofectin technique. The experiments were as follows:(1)Western blot was used to measure the expression level of RACK1.(2)CCK-8, plate colony forming and soft agar colony formation assays were used to detect cell proliferation and growth.(3)Scratch healing experiment was used to detet migration and movement capacity.(4)Cell cycle and apoptosis were measured by flow cytometry.(5)The expression level of VEGF, Bcl-2 and Cyclin D1 were measured by Western blot. Results:(1)Western blot analysis showed that after 48 h of transfection, RACK1 protein expression levels were significantly reduced in four groups which transfected with the specific sh RNA to RACK1(P < 0.05). RACK1 protein expression level transfected with sh RNA1 decreased significantly than the other three groups(P < 0.05), and the expression of RACK1 has no significant change transfected with empty plasmid(P > 0.05).(2)CCK-8, plate colony forming and soft agar colony formation assays showed that the cell proliferation and growth was significantly inhibited(P < 0.05).(3)Scratch healing experiment revealed the migration ability of the cells in the experimental group was significantly decreased(P < 0.05).(4)The number of the experimental group cells in the G0/G1 was increased and the apoptotic rate was also increased(P < 0.05).(5)Western blot results showed that the expression of VEGF, Bcl-2, Cyclin D1 in the experimental group were significantly reduced(P < 0.05). Conclusions:The silencing of RACK1 can inhibit proliferation of lung adenocarcinoma A549 cells and induce apoptosis, negative regulate the expression level of VEGF, Bcl-2 and Cyclin D1.