RNAi silencing of c-Myc inhibits cell migration, invasion, and proliferation in HepG2 human hepatocellular carcinoma cell line: c-Myc silencing in hepatocellular carcinoma cell

Background: Hepatocellular carcinoma (HCC) is the most common type of liver cancer. Although much is known about both the cellular changes that lead to HCC and the etiological agents responsible for the majority of HCC cases, the molecule pathogenesis of HCC is still not well understood. We aimed to determine the effect of c-Myc gene expression on the proliferative, invasive, and migrative capabilities of hepatocellular carcinoma HepG(2) cells. Methods: A plasmid-based polymerase III promoter system was used to deliver and express short interfering RNA targeting c-Myc to reduce its expression in HepG(2) cells. Western blot analysis was used to measure the protein level of c-Myc in HepG(2) cells. The effects of c-Myc silencing on the invasion, motility, and proliferation of HepG(2) cells were assessed using a Transwell chamber cell migration assay system and a growth curve assay, respectively. Results: The data showed that plasmids expressing siRNA against c-Myc significantly decreased its expression in HepG(2) cells by up to 85%. Importantly, pSilencer-c-Myc transfected cells showed a significantly reduced potential in migration, invasion, and proliferation. Conclusion: C-Myc plays an important role in the development of hepatocellular carcinoma. The data show that down-regulating the c-Myc protein level in HepG(2) cells by RNAi could significantly inhibit migration, invasion and proliferation of HepG(2) cells. Thus, c-Myc might be a potential therapeutic target for hepatocellular carcinoma.