MiR-101 functions as a tumor suppressor by directly targeting nemo-like kinase in liver cancer

• MiR-101 expression is down-regulated in hepatocellular carcinomas.
• Ectopic expression of miR-101 suppresses NLK expression in liver cancer cells.
• MiR-101 represses liver cancer cell growth and invasion, in vitro.
• MiR-101 exerts anti-tumor effect by directly targeting oncogenic NLK in liver cancer.

Nemo-like kinase (NLK), an evolutionarily conserved MAP kinase-related kinase, has been reported to be involved in the development of hepatocellular carcinoma (HCC), but the underlying mechanisms leading to oncogenic NLK are poorly understood. A comprehensive microRNA (miRNA) profiling analysis on human HCC tissues identified four downregulated miRNAs that may target NLK. Ectopic expression of miRNA mimics suggested that miR-101 could suppress NLK in HCC cells. Notably, ectopic miR-101 expression repressed cancer cell growth and proliferation and imitated NLK knockdown effect on HCC cells. In conclusion, we suggest that miR-101 functions as a tumor suppressor by regulating abnormal NLK activity in liver.