Previous studies have shown that the HD3 human enterocytic differentiated colon carcinoma cell lines having low $PKC{eta}$ activity did not respond to diacylglycerol and basic FGF by growth and by activation of pp57 MAP kinase, but undifferentiated cell lines exhibiting high $PKC{eta}$ activity did. To confirm a role of $PKC{eta}$ in colonocyte mitogenesis, derivatives of HD3 cell line that stably overexpress a full-length of cDNA encoding the ${eta}_1$ isoform of human PKC were generated. The abundance and activity of $PKC{eta}$ in two of the these cell lines, PKC3 and PKC8 were much higher than those in the C1 control cell line that carries the vector lacking the $PKC{eta}_1;cDNA$ insert. Following exposure to diacylglycerol or basic FGF, proliferation of PKC3 and PKC8 cells increased about 50%; but this effect was not seen with the control C1 cells. Also, in contrast to the control cells, the $PKC{eta}_1-overproducing$ cells displayed activation of pp57 MAP kinase when treated with diacylglycerol and basic FGF as undifferentiated cell lines did. These results provide direct evidence that $PKC{eta}_1$ which plays a key role in mitogenic responses of colon carcinoma cells to diacylglycerol and basic FGF is down-regulated in enterocytic differentiation of colon cells.