AIM: To study the effect and mechanism of chlorophyllin (CHL) inhibiting HT29 cells. METHODS: IC 50 value and growth curve of HT29 cells were detected with MTT method. Apoptosis was detected with Wright-Giemsa staining, FCM and DNA electrophoresis. Telomerase was detected by PCR-ELISA, and protein and mRNA expression of COX-2 gene were detected through RT-PCR and Western blot. RESULTS: CHL inhibited the growth of HT29 in a dose-dependent manner. CHL blocked HT29 cells in G 1 phase but did not induce apoptosis. Different concentration of CHL inhibits the expression of telomerase and COX-2 in HT29 cells. CONCLUSION: CHL inhibits the growth of HT29 cells by inhibiting the expression of telomerase and COX-2 and blocking cells in G 1 phase. [

AIM: To explore the relationship between methylation status of promoter region 5′CpG island and the biological phenotype in human colorectal cancer RKO cell lines. METHODS: RKO cells were treated with selective DNA methyltransferase (DNMTs) inhibitor, 5-Aza-2′-deoxycytidine (5-Aza-CdR), for 72 h. Methylation-specific PCR (MSP), T-A clone and DNA sequence analysis were used to detect 5′CpG island methylation status of p16/CDKN2 tumor suppresor gene. Cell growth, cell cycle arrest and apoptosis were analyzed by MTT, flow cytometry (FCM), fluorescent dye staining and transmission electron microscope. RESULTS: DNMTs inhibitor (5-Aza-CdR) effectively reversed the hypermethylation status of 5′CpG island. The effects of 5-Aza-CdR on cell growth inhibition (P