Cathepsin S silencing induces apoptosis of human hepatocellular carcinoma cells.

This study was to investigate the potential molecular mechanisms underlying the Cathepsin S (CTSS) silencing induced apoptosis of Hepatocellular Carcinoma (HCC) cells with lentivirus-mediated RNA interference. Real-time quantitative PCR and western blot assay were performed to detect the mRNA and protein expression of CTSS, respectively, in 13 HCC cell lines with different metastatic potentials. Results showed MHCC97-H cells had the highest CTSS expression. Therefore, MHCC97-H cells were used in following experiments. Then, lentivirus-mediated RNAi was employed to silence CTSS expression (shCTSS). Annexin V/FITC staining showed NF-κB was activated in shCTSS cells treated with conditioned medium from shCTSS-PAR2 cells. This implies a probable positive correlation between PAR2 and CTSS. In addition, results demonstrated CTSS induced apoptosis of HCC cells and increased their chemosensitivity via regulating NF-κB and activating cleaved caspase-3. Our results indicate that CTSS silencing by lentivirus mediated RNAi can significantly induce apoptosis and chemosensitivity of MHCC97-H cells. This provides an attractive anti-cancer strategy and a novel strategy for the treatment of human HCC.