Knockdown of a Proliferation-inducing Ligand (PRIL) Suppresses the Proliferation of Gastric Cancer Cells

Abstract

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.

Silibinin Inhibits Proliferation, Induces Apoptosis and Causes Cell Cycle Arrest in Human Gastric Cancer MGC803 Cells Via STAT3 Pathway Inhibition

“…Recently, silibinin has received more attention for its anticancer, chemopreventive efficacy and nontoxic roles in humans (Cheung et al, 2010;Deep et al, 2010;Li et al, 2010). Extensive vitro and vivo studies show that the anticancer role of silibinin by regulating cell proliferation, angiogenesis and metastasis in various cancers (Cui et al, 2012;Wang et al, 2013). A variety of signaling pathways associated with cell proliferation have been identified to be involved in the anticancer actions of silibinin (Singh et al, 2004).…”

Tumor necrosis factor superfamily member 13 is a novel biomarker for diagnosis and prognosis and promotes cancer cell proliferation in laryngeal squamous cell carcinoma

“…Previous investigators suggested that TNFSF13 can induce cell proliferation and is overexpressed in some kinds of solid tumor tissues or cells, including head and neck squamous cell carcinoma [12][13][14][15]. In this study, we provide evidence that TNFSF13 can be used as a biomarker for diagnosis and prognosis in LSCC and plays a significant role in LSCC carcinogenesis.…”

RNA Interference: a Promising Therapy for Gastric Cancer

“…As a result, an siRNA specific for APRIL mRNA was designed and transfected different GC cell line cultures. The researchers successfully demonstrated the inhibition of cell viability and colony formation due to cell cycle arrest in the G2/M phase (Cui et al, 2012). These findings provide new clues to the investigation of GC malignant proliferation using the APRIL gene as target.…”

“…The lentiviruses belong to the family of retroviruses and can be used to deliver RNAi (now called shRNA). This shRNA is transfected and integrates into the cell genome, and after gaining stability in prolonged shRNA expression, it keeps the gene silenced (Naldini et al, 1996;Fish and Kruithof, 2004), this being one of the exogenous genes delivery systems preferred by some of the researchers cited in this review (Cui et al, 2012;Liu et al, 2012;Zhou et al, 2012). Several strategies are theoretically proposed for targeting these molecules in order to ensure a better specificity in the target tissue, but tests are necessary which allow demonstrating efficacy in practice.…”