Response of HT115, a highly invasive human colorectal adenocarcinoma cell line, to sodium butyrate treatment and glucose deprivation

Sodium butyrate or glucose deprivation induce a more differentiated phenotype in many cancer cells. The aim of this study was to determine whether the induction effect of butyrate and/or glucose deprivation is dependent, in some way, on the differentiation state of individual cell lines. Sodium butyrate enhanced alkaline phosphatase activity and induced formation of an ultrastructurally more differentiated phenotype in both HT29 and HT115 cell lines. Interestingly, the more invasive HT115 cells responded more strongly to butyrate treatment. On the other hand, the differentiation effect of glucose deprivation was much less prominent in the HT115 cell line in comparison with HT29 cells. Our data confirm the influence of the malignant potential of the cells on their response to treatment with differentiation and apoptosis-inducing agents. Butyrate treatment also enhanced the adhesiveness of HT115 cells. Since E-cadherin was not found in these cells, while the level of CEACAM1 was increased, it is obvious that the CEACAM1 molecules are involved in HT115 cell-cell adhesion.