By a News Reporter-Staff News Editor at Biotech Week -- Fresh data on Small Interference RNAs (siRNAs) are presented in a new report. According to news originating from Wuhan, People's Republic of China, by NewsRx correspondents, research stated, "Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are being widely used as targeted therapy in non-small cell lung cancer (NSCLC), but most cases acquire drug-resistance in 9 months. However, the mechanisms of resistance are still not fully understood."
Our news journalists obtained a quote from the research from the Huazhong University of Science and Technology, "Since it has been demonstrated that EGFR-TKI-mediated repression of downstream signaling cascades and apoptosis induction is a key mechanism through which EGFR-TKIs exert their cytotoxic effects, we reasoned that activation of downstream signaling pathways and changes in the expression of apoptosis-related proteins contribute to the acquired resistance to EGFR-TKIs. We analyzed the protein levels of p-Akt, Bcl-2, Bax between gefitinib-sensitive and gefitinib-resistant lung cancer cell lines and evaluated whether targeting the anti-apoptotic protein Bcl-2 induces cell apoptosis and further sensitizes resistant H1975 cells to gefitinib. The data showed that p-Akt was activated and accompanied by substantial Bcl-2 in the H1975 lung cancer cell line, whereas no evidence was observed in HCC827 cells. Using small interfering RNA (siRNA) to silence Bcl-2 in H1975 cells led to significant downregulation of Bcl-2 protein expression, decreased cell viability in vitro and induced intrinsic apoptosis confirmed by flow cytometry and PARP cleavage. In Bcl-2 siRNA-transfected cells, adding gefitinib further reduced the number of viable cells, induced apoptosis to a greater extent compared to either treatment alone."
According to the news editors, the research concluded: "These preclinical data suggested that downregulation of Bcl-2 by RNAi in the gefitinib-resistant H1975 lung cancer cell line with T790M mutation enhanced the effects of gefitinib and may offer a novel therapeutic strategy for the treatment of NSCLC."
For more information on this research see: Knockdown of the Bcl-2 gene increases sensitivity to EGFR tyrosine kinase inhibitors in the H1975 lung cancer cell line harboring T790M mutation. International Journal of Oncology, 2013;42(6):2094-102 (see also Small Interference RNAs (siRNAs)).
The news correspondents report that additional information may be obtained from M. Zou, Dept. of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Taiwan. Additional authors for this research include S. Xia, L. Zhuang, N. Han, Q. Chu, T. Chao, P. Peng, Y. Chen, Q. Gui and S. Yu.
Keywords for this news article include: Asia, Wuhan, Genetics, Oncology, Proteins, Apoptosis, Treatment, Proteomics, Lung Cancer, Lung Neoplasms, Tyrosine Kinase, Aromatic Amino Acids, Enzymes and Coenzymes, People's Republic of China, Small Interference RNAs (siRNAs).
Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC