Effects of RECQ1 helicase silencing on non-small cell lung cancer cells.

RECQ1, the most abundant one of the human RecQ helicases family, has been identified as a prometastasis gene in breast and cervical cancers. However, the effects of RECQ1 on non-small cell lung cancer (NSCLC) and the underlying molecular mechanisms are still unclear. In the present study, RECQ1 expression (in three NSCLC cell lines and one bronchial epithelial cell line) was detected by real-time quantitative PCR (RT-qPCR). Expression of RECQ1 in A549 cells was knocked down by lentivirus-mediated RNA interference technique (RNAi). The effects of RECQ1 knockdown on cell proliferation, migration and invasion were assessed by Cell Counting Kit-8 (CCK-8) assay and transwell assays. Epithelial-mesenchymal transition (EMT)-associated proteins (E-cadherin, N-cadherin as well as vimentin) were detected by RT-qPCR and western blotting analyses. We found that RECQ1 expression was significantly higher in three NSCLC cell lines than that in a normal human bronchial epithelial cell line. Knocking down RECQ1 significantly suppressed A549 cell proliferation, migration and invasion. The expressions of the epithelial marker, E-cadherin were elevated in both mRNA and protein levels, whereas the expressions of the mesenchymal markers, N-cadherin and vimentin were decreased. Taken together, our findings suggest that RECQ1 may act as an important mediator in promoting lung cancer progression via modulation of the EMT. RECQ1 might represent a potential therapeutic target in NSCLC.