Influences of UPK1A-AS1 on migration and invasion of endometrial carcinoma cells through Wnt/β-catenin signaling pathway
Objective To investigate the expression level of long non-coding RNA UPK1A antisense RNA 1(UPK1A-AS1)in endometrial carcinoma(EC)and the molecular mechanism that regulates the development of EC.Methods Expressions of UPK1A-AS1 in EC were detected in starBase database or by qPCR.Ishikawa cells were allocated into Control group(blank),si-NC group(negative control),si-UPK1A-AS1 group(down-regulation of UPK1A-AS1)and si-UPK1A-AS1+Wnt1 group(down-regulation of UPK1A-AS1 plus activation of Wnt signaling pathway).Cell Counting Kit-8(CCK-8),Wound-healing and Transwell assays were conducted to assess the proliferation,migration,and invasion of Ishikawa cells.Moreover,qPCR and Western blot were carried out to determine the expressions of Wnt1,β-catenin and c-Myc.Results The expressions of UPK1A-AS1 were found to be aberrantly upregulated in EC tissues.Compared with the hEEC cells,UPK1A-AS1 were high-expressed in RL-952,KLE,HEC-1B and Ishikawa cells(P＜0.01).Compared with si-NC group,the cell viability,healing rate and number of invaded cells in si-UPK1A-AS1 group were decreased(P＜0.01).While the cell viability,healing rate and number of invaded cells in si-UPK1A-AS1+Wnt1 group were increased as compared to si-UPK1A-AS1 group(P＜0.01).Besides,si-UPK1A-AS1 group showed lower expressions of Wnt1,β-catenin and c-Myc in both mRNA and protein levels than si-NC group(P＜0.01),but si-UPK1A-AS1+Wnt1 group exhibited higher expressions of Wnt1,β-catenin and c-Myc as compared with si-UPK1A-AS1 group(P＜0.01).Conclusion UPK1A-AS1 activates Wnt signaling to promote the progression and metastasis of EC.The UPK1A-AS1/Wnt/β-catenin/c-Myc axis could be a potential therapeutic target of EC.
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