The role and mechanism of ABL2 in lung cancer / 实用肿瘤学杂志

ABSTRACT

Objective The aim of this study was to investigate the role and mechanism of ABL2 in lung cancer and its mech-anism. Methods The expression of ABL2 in lung cancer and adjacent tissues was detected by Real-Time PCR. A lung adenocarci-noma A549 cell line stably expressing of ABL2 was established,and the changes of cell proliferation and migration ability were detec-ted by MTT,cell migration and colony formation assays. Western blot was used to detect the expression of EMT,apoptosis and PI3K/AKT signaling pathway-related proteins. Results The expression of ABL2 in lung cancer tissues was significantly higher than that in adjacent tissues(P<0. 001). After silencing ABL2 in the A549 cells,compared with the control group,the migration ability of cells was weakened after 48 hours(P<0. 001),the growth rate of cells began to slow down from the third day(P<0. 05),and the average number of clones formed after 15 days also decreased(P<0. 01). The expression of E-cadherin( P<0. 001) was increased in the epithelial cell marker after silencing ABL2,and the expression of stromal cell markers N -cadherin ( P <0. 001),Vimentin ( P <0. 01)and Snail(P<0. 001)was decreased. The expression of apoptosis-related protein Bcl-XL(P<0. 01)was decreased and BAX ( P<0. 001)expression was up-regulated. The expression of PI3K/AKT signaling pathway-associated proteins such as PI3K P110 (P<0. 05),AKT(P<0. 01) and p-AKT( P<0. 05) was significantly decreased. Conclusion Silencing ABL2 gene can promote apoptosis,and inhibit proliferation and migration of lung cancer cells through a PI3K/AKT signaling pathway.