Effect of TNF-α induced protein-2 on the proliferation, apoptosis, migration,and invasion of non-small cell lung cancer H1299 cells

Abstract:

Objective：To investigate the expression of TNF-α-induced protein 2（TNFAIP2） in non-small cell lung cancer （NSCLC） and its effect on cell proliferation，apoptosis，migration，and invasion. Methods：RT-PCR was used to measure the mRNA expression of TNFAIP2 and immunohistochemistry was used to measure the protein expression of TNFAIP2 in NSCLC. The lentivirus-mediated short hairpin RNA of TNFAIP2（shRNA-TNFAIP2） and negative control lentivirus（shRNA-NC） were constructed and were used to infect H1299 cells，and then RT-PCR and Western blot were used to measure the efficiency of infection. Transwell assay was used to measure cell migration and invasion abilities，CCK-8 assay was used to measure proliferative capacity，flow cytometry was used to measure cell apoptosis，and Western blot was used to measure the changes in the protein expression of E-cadherin，N-cadherin，and vimentin. Results：The mRNA and protein expression of TNFAIP2 in NSCLC tissue was significantly higher that that in adjacent tissue. After TNFAIP2 was downregulated by lentivirus，compared with the shRNA-NC group，the shRNA-TNFAIP2 group had significant reductions in the number of migrated cells（170±11 vs. 329±31，P=0.001） and the number of invasive cells（75±10 vs. 135±8，P=0.001）. CCK-8 assay showed that the shRNA-TNFAIP2 group had a significantly lower absorbance value than the shRNA-NC group（P=0.000）；flow cytometry showed that the shRNA-TNFAIP2 group had a significantly higher apoptosis rate than the shRNA-NC group[（18.730±0.490）% vs. （6.570±0.870）%，P=0.000]；Western blot showed that compared with the shRNA-NC group，the shRNA-TNFAIP2 group had reductions in the protein expres－sion of N-cadherin and vimentin and an increase in the protein expression of E-cadherin. Conclusion：TNFAIP2 is highly ex－pressed in NSCLC. Downregulation of TNFAIP2 can inhibit cell proliferation，migration，and invasion，promote cell apoptosis，and re－verse epithelial-mesenchymal transition.