By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Research findings on Biotechnology are discussed in a new report. According to news originating from Jiangsu, People's Republic of China, by NewsRx correspondents, research stated, "NK4, a competitive antagonist for hepatocyte growth factor (HGF) and the Met receptor, is a bifunctional molecule that acts as an HGF antagonist and an angiogenesis inhibitor. The objective of this study was to investigate the anti-tumor effects of NK4 on the cholangiocarcinoma (CCA) cell line HuCC-T1."
Our news journalists obtained a quote from the research from Nanjing Medical University, "We assessed the effects of NK4 on proliferation, invasion, migration, and cell cycle progression in mock-transfected HuCC-T1 clones, empty-vector-transfected clones of HuCC-T1 (Hu-Em), and NK4-transfected clones of HuCC-T1 (Hu-NK4), with HuCC-T1 cells serving as the control cells. Correlated with these effects on cellular functions, the mRNA levels of cyclin D1 and cyclin A were monitored using reverse transcription (RT)-PCR and quantitative PCR, and the corresponding protein levels were monitored using Western blotting. In addition, Met phosphorylation and the activity of its important downstream signaling targets protein kinase B (Akt) and glycogen synthase kinase (GSK)-3 beta were evaluated by Western blotting. Our data indicate that cell proliferation, invasion, and cell cycle progression of the three types of clones were essentially the same, while these processes were stimulated by HGF in HuCC-T1 and Hu-Em cells, but not in Hu-NK4 cells. Moreover, when stimulated with HGF, the increases in mRNA levels of cyclin D1 and cyclin A were accompanied by corresponding increases in protein levels, and the phosphorylation of Met, Akt, and GSK-3 beta was upregulated in HuCC-T1 and Hu-Em cells, compared to the levels in the Hu-NK4 cells. These findings suggest that NK4 gene therapy inhibits HGF/Met-induced growth of human CCA cells by arresting cell cycle progression."
According to the news editors, the research concluded: "It also interferes with Met activation and the downstream phosphatidylinositol-3-kinase/Akt/GSK-3 beta signaling pathway."
For more information on this research see: NK4 Gene Therapy Inhibits HGF/Met-Induced Growth of Human Cholangiocarcinoma Cells. Digestive Diseases and Sciences, 2013;58(6):1636-1643. Digestive Diseases and Sciences can be contacted at: Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands. (Springer - www.springer.com; Digestive Diseases and Sciences - www.springerlink.com/content/0163-2116/)
The news correspondents report that additional information may be obtained from X.X. Ge, Nanjing Medical University, Nanjing Hosp, Clin Lab, Nanjing, Jiangsu, People's Republic of China. Additional authors for this research include Y.L. Wang, Y. Wang, Q.P. Li, H. Yu and L. Miao (see also technology.html">Biotechnology).
Keywords for this news article include: Asia, Biotechnology, Kinase, Jiangsu, Oncology, Gene Therapy, Bioengineering, Cholangiocarcinoma, Enzymes and Coenzymes, People's Republic of China
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