LAUSR

CLDN1 (claudin1) is essential for intercellular junctions and has been reported to be involving in cell migration and metastasis, making it as an oncogene in various cancer types. However, the biological function roles and regulatory mechanisms of CLDN1 in hepatocellular carcinoma (HCC) are still not clarified. In this study, we found down-regulation of miR-29a and up-regulation of CLDN1 in HCC tissues and cell lines. Further found an inverse relation between the expressions of miR-29a and CLDN1 in HCC. Dual-luciferase reporter assay indicated that miR-29a regulated the expression of CLDN1 by binding to its 3' untranslated region (3'UTR). Knockdown of CLDN1 led to decrease in tumor cell growth and migration capacities in vitro and in vivo. While overexpression of miR-29a suppressed tumor growth and migration, these effects could be reversed by re-expressing CLDN1. Taken together, out data suggested that miR-29a may regulate tumor growth and migration by targeting CLDN1, providing promising therapeutic targets for HCC.