AIM:To investigate the cellular effects of hybrid polarcompound hexamethylene bisacetamide (HMBA) on thegrowth and apoptosis of human hepatocellular carcinomacells and to provide the molecular mechanism forpotential application of HMBA in the treatment of livercancer.METHODS:Effects of HMBA on the growth of humanhepatocellular carcinoma SMMC-7721 cells were assayedby MTT chronometry.Apoptosis induced by HMBA wasdetected by phase-contrast microscopy,flow cytometry,propidium iodide staining and immunocytochemicalanalysis.RESULTS:The growth of SMMC-7721 cells was significantlyinhibited by HMBA,and the growth inhibitory rate was51.1%,62.6%,68.7% and 73.9% respectively aftertreatment with 5.0,7.5,10.0 and 12.5 mmol/L of HMBA.In the cells treated with 10 mmol/L of HMBA for 72 h,thepopulation of cells at sub-G_1 phase significantly increased,and the apoptotic bodies and condensed nuclei weredetected.Moreover,treatment of SMMC-7721 cells with10 mmol/L of HMBA down-regulated the expression of Bcl-2 anti-apoptotic protein,while slightly up-regulated the levelof pro-apoptotic protein Bax.CONCLUSION:Treatment with 10.0 mmol/L of HMBA cansignificantly inhibit the growth and induce apoptosis ofhuman hepatocellular carcinoma SMMC-7721 cells bydecreasing the ratio of Bcl-2 to Bax. AIM: To investigate the cellular effects of hybrid polarcompound hexamethylene bisacetamide (HMBA) on the growth and apoptosis of human hepatocellular carcinoma cells and to provide the molecular mechanism for potential application of HMBA in the treatment of liver cancer. METHODS: Effects of HMBA on the growth of human hepatocellular carcinoma SMMC-7721 cells were assayed by MTT chronometry. Apoptosis induced by HMBA wasdetected by phase-contrast microscopy, flow cytometry, propidium iodide staining and immunocytochemicalanalysis. RESULTS: The growth of SMMC-7721 cells was significantly inhibited by HMBA, and the growth inhibition rate was 51. 1%, 62.6%, 68.7% and 73.9% respectively aftertreatment with 5.0, 7.5, 10.0 and 12.5 mmol / L of HMBA.In the cells treated with 10 mmol / L of HMBA for 72 h, thepopulation of cells at sub-G_1 phase significantly increased, and the apoptotic bodies and condensed nuclei were detached. Moreover, treatment of SMMC-7721 cells with 10 mmol / L of HMBA down-regulated the expression of B cl-2 anti-apoptotic protein, while slightly up-regulated the level of pro-apoptotic protein Bax. CONCLUSION: Treatment with 10.0 mmol / L of HMBA cansignificantly inhibit the growth and induce apoptosis ofhuman hepatocellular carcinoma SMMC-7721 cells by deccreasing the ratio of Bcl -2 to Bax.