Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8549, Japan.
The anti-cancer potential of vitamin K(2) (VK(2)) in hepatoma has gained considerable attention but the underlying mechanisms are unclear. Treatment of HuH7 hepatoma cells with VK(2) produced a normal liver phenotype. Following treatment of cells with VK(2), there was an increase in gap junctional intercellular communication activity, accompanied by up-regulation of connexin 32 (Cx32), dominantly expressed in normal hepatocyte. In contrast, Cx43 expression was inhibited. Moreover, the effect of VK(2) on Cx32 was abolished by over-expression of Cx43. Taken together, we propose that the anti-tumor effect of VK(2) is at least partly due to a decrease in Cx43 promoter activity.