Expression of SPHK1 in lung adenocarcinoma and its effect on epithelial mesenchymal transition in A549 cell line

YAN Dong-xing; YUAN Xiao-mei; WANG Jin-hui

doi:10.13820/j.cnki.gdyx.20242127

Abstract：Objective To investigate the expression of SPHK1 in lung adenocarcinoma and its effects on A549 cell proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT).Methods Transcriptional data from 515 lung adenocarcinoma samples and 59 normal lung tissues were downloaded from the UALCAN database to analyze SPHK1 expression levels and their correlation with patient survival rates.Western blot and qPCR were used to measure SPHK1 protein and mRNA expression in lung adenocarcinoma cell lines(H322 and A549)and normal bronchial epithelial cells(BEAS-2B).A549 cells were divided into si-SPHK1 knockdown group,si-NC control group,and blank control group.CCK-8,scratch,and Transwell assays were employed to assess changes in proliferation,migration,and inva-sion.EMT markers(E-cadherin,N-cadherin,and vimentin)were evaluated via Western blot and qPCR.Results SPHK1 mRNA levels in adenocarcinoma tissues were significantly higher than in normal tissues[8.467(4.626,15.719)vs.5.998 3.948,7.926),P<0.001].Patients with high SPHK1 expression had a median survival time of 69 months,compared to 108 months for those with low expression(HR=1.5,P<0.001).SPHK1 protein and mRNA levels were al-so significantly elevated in H322 and A549 cells compared to BEAS-2B(P<0.05).Knockdown of SPHK1 significantly inhibited A549 cell proliferation,migration,and invasion.E-cadherin levels increased significantly in the si-SPHK1 group,while N-cadherin and vimentin levels decreased compared to controls.Conclusion SPHK1 is significantly over-expressed in lung adenocarcinoma and may promote cell proliferation,migration,and invasion through EMT processes.SPHK1 could serve as a potential therapeutic target for lung adenocarcinoma.