Objective: To investigate the effect of LncRNA DLG1-AS1 on the proliferation and metastasis of papillary thyroid carcinoma(PTC) cells, and further to explore its mechanism. Methods: PTC cells TPC1,KTC-1,B-CPAP,HTori-3 and normal follicular cell Nthy-ori3-1 were used to detect DLG1-AS1 and miR-203 expressions by real time quantitative polymerase chain reaction(qRT-PCR) method. B-CPAP cells were divided into blank group, NC group(transfected pcDNA3.1-vector and negative control inhibitor), shDLG1-AS1 group(transfected pcdna 3.1-shDLG1-AS1), shDLG1-AS1+miR-203 inhibitor group(transfected pcdna3.1-shDLG1-AS1 and miR-203 inhibitor). The proliferation and invasion, migration activities of cells were detected by CCK-8 assay and transwell method. Western blotting was used to detect the relative expression of epithelial-mesenchymal transition(EMT) related proteins. The luciferase report was used to analyze the target relationship between DLG1-AS1, miR-203, and ZEB2. Results: qRT-PCR results showed compared with Nthy-ori3-1 cells, the relative expression of DLG1-AS1 in TPC1, KTC-1, B-CPAP and HTori-3 cells was increased, while the relative expression of miR-203 was decreased(P<0.05).B-CPAP cells with the highest relative expression of DLG1-AS1 were selected for follow-up study. Compared with blank group and NC group, the proliferation, migration and invasion of shDLG1-AS1 group cells were decreased, while the expression of ZEB2, N-cadherin, vimentin, β-catenin protein was down-regulated, and the expression of E-cadherin was up-regulated(P<0.05). Compared with shDLG1-AS1 group, shDLG1-AS1+miR-203 inhibitor group showed a reversal of cell proliferation, migration and invasion, while the expression of ZEB2, N-cadherin, vimentin, β-catenin protein was up-regulated and the expression of E-cadherin was down-regulated(P<0.05). DLG1-AS1 could directly regulate miR-203, and ZEB2 was the downstream target gene of miR-203. Conclusion: By combining with miR-203,LncRNA DLG1-AS1 eliminates the inhibition of miR-203 to ZEB2 expression, promotes the EMT of PTC cells, which may be an important mechanism of PTC malignant growth and metastasis.
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