Overexpression of SLFN5 induced the epithelial-mesenchymal transition in human lung cancer cell line A549 through β-catenin/Snail/E-cadherin pathway.

In this study, overexpression or knockdown of SLFN5 gene were induced by lentiviral transfection in human lung cancer cell line A549, then the EMT of A549 was detected by green fluorescent protein labeling method, the migrative and invasive abilities were evaluated via transwell and wound-healing tests in vitro and chick chorioallantoic membrane inoculation in vivo, and the possible mechanism was studied by quantitative real-time PCR and Western blotting. Our results demonstrated that overexpression of SLFN5 promoted the morphology transformation of A549 from epithelial to mesenchymal, as well as migration and invasion. However, knockdown of SLFN5 resulted in the opposite results. Moreover, with the development of EMT after SLFN5 was overexpressed, A549 exhibited enhanced translocation of β-catenin from membrane to cytoplasm or nucleus, with higher level of EMT-related transcription factor Snail, and lower expression of adhesin E-cadherin. Together these results suggest that SLFN5 may act as a synergist in lung cancer cell tumorigenesis and progression, providing a potential target for developing drugs for lung cancer therapy in future. PMID: 31472120 [PubMed - as supplied by publisher]
Source: European Journal of Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Eur J Pharmacol Source Type: research