Asian Pacific J Cancer Prev, 13, 633-636
IntroductionGastric cancer (GC), the second most common cause of cancer-related death in the world, can develop in any part of the stomach and spread throughout the stomach and to other organs. There are about 1,000,000 new diagnoses and 800,000 deaths worldwide each year (Kamangar et al., 2006). The 5-year survival rate for curative surgical resection ranges from 30-50% for patients with stage II disease and from 10-25% for patients with stage III disease. The operative mortality rate for patients undergoing curative surgical resection at major academic centers is less than 3% (http://emedicine.medscape.com/ article/278744-overview). In this scenario, understanding the molecular mechanisms underlying the initiation and progression of GC is important for prevention, early diagnosis and identifying novel therapeutic and clinical targets for GC (Li et al., 2009;Yu et al., 2009).A proliferation-inducing ligand (PRIL) (also known as TALL-2, TRDL1, or TNFSF13) is a member of tumor necrosis factor (TNF) family. It was originally identified in cell lines and primary samples from various tumor lesions in 1998 and named for its capacity to stimulate the proliferation of tumor cells (Hahne et al., 1998). In contrast to most TNF family members, APRIL is processed in the Golgi apparatus into the active soluble form by a furin convertase (Lopez-Fraga et al., 2001). APRIL is expressed by a subset of immune cells that also produce B-cell activating factor (BAFF): monocytes, macrophages, Moreover, the cell cycle was arrested at G2/M phase, elucidating the mechanism underlying the inhibitory effect of siRNA on cell proliferation. Conclusions: Our study indicated that PRIL functions in promoting cell growth, and lentivirus-mediated PRIL gene knockdown might be a promising strategy in the treatment of gastric cancer.