Targeting the Mutant Region in K-RAS by RNA Interference Controlling Cell Proliferation and Programmed Cell Death in Liver Cancer Cells.

Background Hepatocellular carcinoma (HCC) is a high-incidence and significant cause of cancer globally. HCC the world's third most common death-related sixth tumor. In HCC, various cellular signaling activated to ensure malignancy transformation, angiogenesis, metastasis. The efficient pathway in mitogen-activated protein kinase (MAPK), which controls regulates apoptosis. mutant k-ras gene led activation RAS with GTPase activity, stimulated hepatocellular proliferation transformation. Here we aim investigate correlation between knock-down evaluation in-vitro. 
 Material Methods We used HepG2 cell line direct connection expression profile RAF/MEK using respective siRNA antagonist k-ras. Results Interestingly, altered morphology number living cells. addition, transfection cells firstly designed successfully reduced relative Raf-1 Mek1, downstream targets signaling. Furthermore, interleukin 8 (IL-8) 6 (IL-6) were monitored fluids media at different time points following transfection. Both IL-6 Il-8 production significantly increased transfected targeting Conclusion Our findings provide evidence for influential role mutated development suggest possible regulation this as potential treatment HCC.