RESUMEN
The aim of the present study was to investigate the effect of hedgehoginteracting protein antisense RNA 1 (HHIPAS1) on epithelialmesenchymal transition (EMT) and cellular stemness of human lung cancer cells by regulating the microRNA (miR)1533p/PCDHGA9 axis. Reverse transcriptionquantitative PCR was used to compare the expression of HHIPAS1 in lung cancer and adjacent normal lung tissues. In addition, the correlation of HHIPAS1 with Ecadherin, Vimentin, Ncadherin and Twist1 was analyzed. HHIPAS1 overexpression vector was transfected into lung cancer A549 and NCIH1299 cell lines. Cell Counting Kit8 and Transwell and clonogenic assays were used to detect the proliferation, invasion and clonogenesis of the lung cancer cells, respectively. The associations among HHIPAS1, miR1533p and PCDHGA9 were predicted by bioinformatics analysis and verified by a dualluciferase reporter system. The results showed that the expression of HHIPAS1 in lung cancer tissues was significantly lower than that in normal tissues (P<0.001). HHIPAS1 was positively correlated with Ecadherin and negatively correlated with Vimentin, Ncadherin and Twist1. HHIPAS1 overexpression inhibited the proliferation, invasion and clonal formation of the A549 and NCIH1299 cells. The luciferase reporter system verified that HHIPAS1 could adsorb miR1533p and that PCDHGA9 was the target gene of miR1533p. A549 cells were transfected with HHIPAS1 overexpression vector and miR1533p mimic, and the miR1533p mimic had a mitigating effect on HHIPAS1 inhibition (P<0.001). In conclusion, HHIPAS1 inhibits the EMT and stemness of lung cancer cells by regulating the miR1533p/PCDHGA9 axis. Thus, HHIPAS1 may be a new potential target for lung cancer treatment.