Abstract
Tumor protein D52-like 2 (TPD52L2) has been commonly described as a protein involved in tumorigenesis, according to its name. However, its pathological function remains under investigation. In the present study, TPD52L2 was found to be widely expressed in several gastric cancer cell lines. An efficient knockdown of TPD52L2 by a specific short hairpin RNA (shRNA) loaded in lentivirus resulted in a remarkable reduction in cell proliferation in both MGC80-3 and SGC-7901 cell lines with high TPD52L2 expression, but a slight or little reduction in the proliferation of MKN-28 and AGS cells with low TPD52L2 expression. Further analysis by flow cytometry revealed that the cell cycle was primarily blocked in the G0/G1 phase, especially in the sub-G1 phase by TPD52L2 silencing, implying its possible roles in cell cycle control and apoptosis. Knockdown of TPD52L2 caused a cleavage of PARP in MGC80-3 cells. Their study suggests that TPD52L2 might promote gastric carcinogenesis, and could be a promising target with respect to developing new therapeutic strategies to treat gastric cancer.