By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Investigators publish new report on Biotechnology. According to news reporting originating in Nanning, People's Republic of China, by NewsRx journalists, research stated, "CD59, belonging to membrane complement regulatory proteins (mCRPs), inhibits the cytolytic activity of complement and is overexpressed in many types of solid cancers. The aim of the present study was to detect the expression of CD59 in non-small cell lung cancer (NSCLC) and to investigate the relationship between decreased CD59 expression and tumorigenesis of NSCLC by transfecting recombinant retrovirus encoding shRNA targeting human CD59 into the human NSCLC cell line NCI-H157."
The news reporters obtained a quote from the research from Peoples Hospital, "CD59 expression in NSCLC was detected by immunocytochemistry (IHC). In the human NSCLC cell line NCI-H157, CD59 mRNA and protein expression suppressed with lentivirus-mediated RNAi was confirmed by using RT-PCR and western blotting, respectively. The proliferation and apoptosis of NCI-H157 cells was measured by using MTT assay and FACS. The resistance to complement cracking ability was detected by LDH assay. Caspase-3 expression in cells was assessed by IHC. Bcl-2 and Fas protein was determined by western blotting both in vitro and in vivo. CD59 is overexpressed in human NLCLC cancer. In NCI-H157 cells, lentivirus-mediated RNAi significantly reduced both CD59 mRNA and protein expression, which resulted in suppressing cell proliferation and increasing cell apoptosis. When incubated with fresh normal human serum (8%, v/v) for 1 h at 37 C, the cell viability was decreased and cell apoptosis was increased in siCD59-infected NCI-H157 cells compared to siCD59-C-infected cells. Reduced CD59 expression led to increased expression of caspase-3 and Fas and decreased expression of Bcl-2. Furthermore, the nude mouse tumor graft weight was significantly decreased and survival rate was significantly increased in the siCD59 group. CD59 is overexpressed in human NLCLC. CD59 silencing in NSCLC cancer cells via retrovirus-mediated RNAi can enhance complement-mediated cell apoptosis, inhibiting the growth of NSCLC."
According to the news reporters, the research concluded: "CD59 may serve as a potential target for gene therapy in NSCLC."
For more information on this research see: CD59 is overexpressed in human lung cancer and regulates apoptosis of human lung cancer cells. International Journal of Oncology, 2013;43(3):850-858. International Journal of Oncology can be contacted at: Spandidos Publ Ltd, Pob 18179, Athens, 116 10, Greece (see also technology.html">Biotechnology).
Our news correspondents report that additional information may be obtained by contacting B.J. Li, Peoples Hosp Guangxi, Nanning 530000, Zhuang Autonomo, People's Republic of China. Additional authors for this research include H. Lin, J. Fan, J. Lan, Y.L. Zhong, Y. Yang, H. Li and Z.W. Wang.
Keywords for this news article include: Asia, Biotechnology, Nanning, Oncology, Apoptosis, Lung Cancer, Bioengineering, Lung Neoplasms, Cancer Gene Therapy, People's Republic of China
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