Effects Of Lentivirus-mediated RNAi Inhibiting TPD52L2on Proliferation Of Human Lung Adenocarcinoma Cell Line A549

ObjectiveLung cancer is a major cause of cancer-related death. TPD52family has been commonly described as a protein involved in tumorigenesis in several cancers. However, its biological function remains under investigation in lung cancer.MethodsIn this study, to elucidate the functional role of TPD52L2in lung cancer, we employed lentivirus-mediated short hairpin RNA (shRNA) to knock down TPD52L2in one lung cancer cell line A549. And then we observe the effects of lentivirus-mediated RNAi inhibiting TPD52L2on proliferation of A549, as determined by MTT and colony formation assays.ResultsThe lv-shTPD52L2and1v-shCon recombinant lentiviruses were successfully constructed. We observeed that an efficient knockdown of TPD52L2after lentivirus infection resulted in a remarkable reduction in cell the proliferation and colony formation in A549cell lines. Furthermore, knockdown of TPD52L2led to an accumulation of cells in the G2/M phase of the cell cycle by flow cytometry. ConclusionThis investigation indicates that TPD52L2plays an essential role in the growth of lung cancer cells in vitro, which may contribute to provide gene therapy for human lung adenocarcinoma treatment.