lncAKR1C2通过调节微小RNA-137对肺腺癌细胞增殖、迁移和免疫逃逸的影响OA

Objective:To investigate the effects of long non-coding RNA(lncRNA)lncAKR1C2 on the prolifer-ation,migration and immune escape of lung adenocarcinoma cells by regulating microRNA(miR)-137.Methods:The expression levels of lncAKR1C2 in lung adenocarcinoma tissues were analyzed using the ICGC database.Real-time quantitative PCR(qRT-PCR)was used to examine lncAKR1C2 expression in lung adenocarcinoma cell lines(H1975,H1650,H1299,and A549).A549 cells were divided into two groups:a si-NC group(transfected with si-NC)and a si-lncAKR1C2 group(transfected with si-lncAKR1C2).The proliferation of A549 cells in each group was assessed by the MTS assay,and the migration of A549 cells was assessed by the wound healing assay.Western blot analysis was used to examine the expression of the immune escape proteins programmed death-ligand 1(PD-L1),cy-totoxic T-lymphocyte-associated protein 4(CTLA-4),B7 homolog 3(B7-H3),and B7 homolog 4(B7-H4)in A549 cells.A dual-luciferase reporter assay was used to verify the targeting relationship between lncAKR1C2 and miR-137.The ICGC database was used to analyze the correlation between lncAKR1C2 and miR-137 expressions in lung adeno-carcinoma tissues.qRT-PCR was used to determine the expression level of miR-137 in A549 cells in each group.Re-sults:Compared with normal lung tissue,lncAKR1C2 expression was significantly increased in lung adenocarcinoma tissue(P＜0.01).Compared with bronchial epithelial BEAS-2B cells,lncAKR1C2 expression was significantly in-creased in H1975,H1650,H129 9,and A549 cells(all P＜0.01).Compared with the si-NC group,the proliferation a-bility of A549 cells in the si-lncAKR1C2 group was reduced(P＜0.01),the cell migration rate was significantly de-creased(P＜0.01),and the expression of PD-L1,CTLA-4,B7-H3,and B7-H4 proteins was significantly decreased(P＜0.01).lncAKR1C2-WT had a targeting relationship with miR-137(P＜0.01).lncAKR1C2-WT is negatively correlated with miR-137 expression in lung adenocarcinoma tissues(P＜0.01).Compared with the si-NC group,miR-137 expression in A549 cells in the si-lncAKR1C2 group was significantly increased(P＜0.01).Conclusion:In-terference in lncAKR1C2 expression can reduce the proliferation and migration ability of A549 cells and inhibit their immune escape,and its molecular mechanism may be achieved by regulating miR-137 expression.