[Knockdown of long non-coding RNA actin filament-associated protein 1 antisense RNA1 (AFAP1-AS1) inhibits epithelial-mesenchymal transition, invasion and migration of TPC-1 papillary thyroid cancer cells].

Objective To detect the expression of long non-coding RNA (lncRNA) actin filament-related protein 1 antisense RNA1 (AFAP1-AS1) in papillary thyroid carcinoma tissue, and to investigate the effects of the knockdown of AFAP1-AS1 in TPC-1 papillary thyroid carcinoma cells on cell epithelial-mesenchymal transition (EMT) and related molecular mechanism in TPC-1 cells. Methods Real-time quantitative PCR was used to detect the expression of lncRNA AFAP1-AS1 in 60 cases of papillary thyroid carcinoma tissues. RNA interfering (RNAi) was used to knockdown AFAP1-AS1 in TPC-1 cells. TPC-1 cells were divided into AFAP1-AS1 knockdown (shAFAP1-AS1) group, negative control RNA (shNC) group and untransfected control group. The colony-formation assay, TranswellTM invasion and scratch healing assays were employed to detect the colony-forming ability, cell invasion ability and cell migration ability of TPC-1 cells, respectively. After knockdown of AFAP1-AS1, real-time quantitative PCR and Western blot analysis were used to detect the mRNA and protein levels of E-cadherin, vimentin, β-catenin and snail2, respectively. Results Compared with the paracancerous tissue, the expression level of AFAP1-AS1 mRNA in the papillary thyroid carcinoma tissue significantly increased. Knockdown of AFAP1-AS1 significantly reduced the colony-forming ability, invasion and migration ability of TPC-1 cells. Compared with shNC group and control group, knockdown of AFAP1-AS1 significantly reduced the mRNA and protein expression of snail2, vimentin and β-catenin. In contrast, the mRNA and protein expression of E-cadherin increased considerably. Conclusion The lncRNA AFAP1-AS1 is highly expressed in papillary thyroid carcinoma tissue. After knockdown of AFAP1-AS1 in TPC-1 cells, the colony-forming ability, invasion and migration ability of cancer cells are significantly down-regulated, which may be related to the inhibition of EMT.