New Findings on Cancer Gene Therapy Described by Investigators at Peking University (Knockdown of WWP1 inhibits growth and induces apoptosis in hepatoma carcinoma cells through the activation of caspase3 and p53)
By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Fresh data on Biotechnology are presented in a new report. According to news reporting from Beijing, People's Republic of China, by NewsRx journalists, research stated, "The activation of oncogenes and the loss of tumor suppressor genes are believed to play critical roles in the pathogenesis of human hepatocellular carcinoma (HCC). The human WW domain containing E3 ubiquitin protein ligase 1 (WWP1) gene is frequently amplified in prostate and breast cancers, however, its role in cancer has not yet been extensively studied."
The news correspondents obtained a quote from the research from Peking University, "Especially, the role of WWP1 in HCC has not yet been studied. Firstly, we analyzed the expression of WWP1 in HCC samples. We found that protein levels of WWP1 are higher in most HCC cancerous tissues as compared with their matched adjacent non-tumor tissues. Additionally, the WWP1 mRNA was also amplified in all 7 HCC tissues. Knockdown of the endogenous WWP1 using small interfering RNA further showed that deficiency of WWP1 suppressed cell growth and caused apoptosis in HCC cells. Knocking down WWP1 promoted cleaved caspase3 protein and p53 expression in HCC cells, and caspase3 inhibition could prevent cell apoptosis induced by the knockdown of WWP1. All together these results indicate that protein levels of WWP1 in most HCC tissues are higher than non-tumor tissues, and knockdown of WWP1 inhibits growth and induces apoptosis in HCC cells through the activation of caspase3 and p53."
According to the news reporters, the research concluded: "Therefore, WWP1 gene might be a potential molecular target of HCC."
For more information on this research see: Knockdown of WWP1 inhibits growth and induces apoptosis in hepatoma carcinoma cells through the activation of caspase3 and p53. Biochemical and Biophysical Research Communications, 2014;448(3):248-254. Biochemical and Biophysical Research Communications can be contacted at: Academic Press Inc Elsevier Science, 525 B St, Ste 1900, San Diego, CA 92101-4495, USA. (Elsevier - www.elsevier.com; Biochemical and Biophysical Research Communications - www.elsevier.com/wps/product/cws_home/622790)
Our news journalists report that additional information may be obtained by contacting Q. Cheng, Peking University, Hlth Sci Center, Res Center Aging, Dept. of Biochem & Mol Biol, Beijing 100191, People's Republic of China. Additional authors for this research include X.X. Cao, F.W. Yuan, G.D. Li and T.J. Tong (see also Biotechnology).
Keywords for this news article include: Asia, Biotechnology, Beijing, Genetics, Oncology, p53 Gene, Apoptosis, Cancer Gene Therapy, Hepatocellular Carcinoma, People's Republic of China
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