Beta1,4-galactosyltransferase1 (beta1,4GT1) is localized both in the Golgi complex
and on the cell surface. In our previous study, we first reported that beta1,4GT1
was associated with cycloheximide-induced apoptosis in human hepatocarcinoma cells.
In this study, we transfected constitutively active protein kinase B (Gag-PKB), a
central mediator of anti-apoptotic signals transduced by the PI3-kinase, into SMMC-7721
human hepatocarcinoma cells, and examined its effect on apoptosis and beta1,4GT1 activity.
Flow cytometry analysis showed that apoptosis was inhibited in Gag-PKB transfected
SMMC-7721 cells. At the same time, beta1,4GT1 mRNA level and enzyme activities were
downregulated in these cells, consistent with which, the content of beta1,4 Gal branch
in the glycoconjugates was decreased in stably transfected cells. Cotransfection of
beta1,4GT1 promoter/luciferase reporter and Gag-PKB decreased the luciferase reporter
activity in a dose-dependent manner, indicating that the differences in mRNA levels
might be regulated through promoter function. All these findings suggested that changes
of beta1,4GT1 activity might be involved in apoptotic pathway in hepatocarcinoma cells.