Results: The oxaliplatin induced apoptosis was significantly increased in cells with defective Pokemon. Western blots showed www.selleckchem.com/products/gsk1120212-jtp-74057.html that p53 expression and phosphorylation were significantly increased in Pokemon defective cells, thereby initiating the mitochondria-mediated and death receptor-mediated apoptotic pathways. In the mitochondria-mediated pathway, expression of pro-apoptotic Bcl-2 family members (including Bad, Bid, Bim and Puma) as well as AIF and cytochrome C was increased in HepG2 si-Pokemon cells. In addition, upon oxaliplatin treatment
of Pokemon-silenced cells, the FAS receptor, FADD and their downstream targets caspase-10 and caspase-8 were activated, causing increased release of caspase-8 active fragments p18 and p10. Increased activated caspase-8-mediated cleavage and activation of downstream effector caspases such as caspase-9 and caspase-3 was observed in HepG2 si-Pokemon cells as compared to control. Conclusion: Pokemon might serve as an important mediator of crosstalk between intrinsic and extrinsic apoptotic pathways in HCC cells. Moreover,
our findings suggest that Pokemon could be an attractive Ixazomib price therapeutic target gene for human cancer therapy. Key Word(s): 1. Pokemon; 2. HCC; 3. Caspase; Presenting Author: HOSSAIN JABBARI Additional Authors: HOSSAIN JABBARI Corresponding Author: HOSSAIN JABBARI Affiliations: Medical University of Wien Objective: Hepatocellular necrosis, inflammatory infiltrates and fibrosis of liver are histological characteristics of chronic hepatitis C (CHC) infection. Despite fluctuations in the first two, fibrosis of liver, if patient untreated, has a progressive nature and could lead to hepatic microcirculatory and cellular damage and dysfunction. Therefore, determining the degree of liver fibrosis through invasive or non-invasive methods is crucial to the understanding of the natural history of chronic hepatitis C1. There is a couple of risk factors, both host- and virus- related factors, which are associated with the accelerated rate of liver www.selleck.co.jp/products/Rapamycin.html fibrosis in patients with CHC infection. The
most important are consuming excessive quantities of alcohol, being over 40 years of age at the time of HCV diagnosis, co-infections (with human immunodeficiency virus (HIV) and/ or hepatitis B virus (HBV), co- morbid conditions (organ transplantation, obesity, liver steatosis and diabetes mellitus), being male, smoking, carrying special single nucleotide polymorphisms, and infection with some HCV genotypes1, 2, 3. All of these risk factors, singly or collectively, could contribute to liver fibrosis progression. Based on our knowledge, there is no indicator to show the global situation of fibrosis in patients with chronic HCV infection. The aim of this study is to present a new indicator to evaluate HCV fibrosis in the community.