Julien D.C., Giri A., Papasani M., Murdoch G., Hrdlicka P., Hill R.A.
University of Idaho, US
Keywords: K-Ras, pancreatic cancer, siRNA
Cancer of the pancreas is a leading cause of cancer-related mortality. Chemotherapeutic drugs used to treat pancreatic cancers are toxic and minimally effective, yielding a 1-4% 5-year survival rate after initial diagnosis. Approximately 90% of pancreatic cancers possess point mutations in the K-Ras proto-oncogene. Point mutations in the K-Ras gene cause the K-Ras protein to become stuck in the “on” GTP bound conformation, leading to constitutive activation. Small interfering RNA (siRNA) against mutated K-Ras (mK-Ras) may be a potential therapeutic option for the treatment of pancreatic cancers. In this study, four pancreatic cancer cell lines were used: two that are homozygous for an mK-Ras point mutation, one that is heterozygous and one that has the wild genotype (wK-Ras). Cells were transfected with Lipofectamine and either scrambled siRNA or mK-Ras siRNA and K-Ras gene expression quantified at 24, 48, or 72 h after transfection. Data from mK-Ras genotypes showed a significant down-regulation of mK-Ras compared to cells transfected with scrambled siRNA. Data for the wK-Ras cell line, showed no significant change in wK-Ras mRNA throughout all time-points. These data provide initial proof-of-priciple that siRNA may be a successful treatment for knockdown of mK-Ras and may serve as a valid approach to treating cancers with K-Ras point mutations.
Journal: TechConnect Briefs
Volume: 3, Nanotechnology 2010: Bio Sensors, Instruments, Medical, Environment and Energy
Published: June 21, 2010
Pages: 401 - 404
Industry sector: Medical & Biotech
Topics: Biomaterials, Cancer Nanotechnology
ISBN: 978-1-4398-3415-2