Our study revealed that the expression of the MTA1gene was remarkably decreased after the PDCD4 gene transfection.

In the migration and Matrigel invasion assay, we discovered that the MHCC-97H cells migrated to the lower surface were greatly decreased after PDCD4 gene transfection. A study on a human acute myeloid leukemia (AML) cell line NB4 demonstrated that Knockdown of PDCD4 by RNA interference (siRNA) leads to induction of c-myc, suggesting that c-myc maybe a potential down-stream target of PDCD4[7]. MTA1 is an integral subunit of nucleosome remodeling and histone deacetylation (NuRD) complex which contains both histone deacetylase and nucleosome remodeling activity. It has been shown to be overexpressed in metastatic carcinomas. Recent studies on rat fibroblasts cells revealed that MTA1 is one of the essential first down-stream effectors of the c-myc oncoprotein. Activation of c-myc causes induction of the MTA1 expression [34]. In MHCC-97H cells stably Selleckchem CB-839 transfected with the PDCD4, activity of c-myc maybe inhibited and the gene expression of MTA1 is further blocked. Metastasis is a multistep process. Cell migration and invasion are essential for tumor progression and metastasis. Matrigel is a reconstituted

basal membrane with most components of extracellular membrane. Malignant cells have to degrade the surrounding ECM before spread [35]. Metastatic potential of MHCC-97H cells had been found to be correlated to the number of cells migrated in the migration and invasion assay [14]. In summary, we showed that the expression of PDCD4 was inversely correlated to the metastatic potentials of HCC cells. PDCD4

see more effectively blocked the proliferation rate, decreased the gene expression of metastasis associated protein1, and inhibited the migration and invasion activities of MHCC-97H cells. These results demonstrate that PDCD4 might be a novel suppressor to metastatic potential of HCC cells. By our knowledge, this was the first observation to investigate the effects of PDCD4 on metastatic potential of HCC cells. Further studies are required to confirm these findings in vivo. Acknowledgements We thank Chuanxi Wang at Key Laboratory of Biotech-Drugs Ministry of Health of Shandong Academy of Medical Sciences for his excellent technical support and Zunchang Liu at Artificial Cells and Organs Research Center of McGill University Methane monooxygenase for his critical reading of the manuscript. References 1. Kirk GD, Bah E, Montesano R: Molecular epidemiology of human liver cancer: insights into etiology, pathogenesis and prevention from The Gambia. West Africa. Carcinogenesis 2006, 27: 2070–2082.CrossRefPubMed 2. Lai EC, Lau WY: Spontaneous Rupture of Hepatocellular Carcinoma: A Systematic Review. Arch Surg 2006, 141: 191–198.CrossRefPubMed 3. Li X, Pan Y, Fan R, Jin H, Han S, Liu J, Wu K, Fan D: Adenovirus-delivered CIAPIN1 small interfering RNA inhibits HCC growth in vitro and in vivo. Carcinogenesis 2008, 29: 1587–1593.