| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
The role of gap junction in development ,progression and metastasis of gastric cancer was investigated in this project. First, gap junction formation was confirmed to be made during the culture and differentiation of gastric mucosal cells originated from rabbit fetus. Next, the expression of gap junction in the gastric cancer cell lines was examined and there was no expression during the culture and proliferation of the gastric cancer cell lines. To investigate the mechanism of progression and invasion of gastric cancer to the normal tissues, the expression of gap junction as well as proliferation was investigated using the coculture of normal gastric mucosal cells and gastric cancer cells. There was seen a gap junction between two cells and the proliferation activity of gastric cancer cells was decreased. At that time, it was considered that this project can be finished. Therefore, next, it was investigated how the expression of gap junction was regulated. Furthermore, it was confirmed that Wnt signaling including WNT8B and WNT10B was increased during the culture of gastric cancer cells. It seems that there is a reciprocal change between Wnt signaling and the expression of gap junction. Also, FRAT2, a mediator of Wnt signaling, was increased in parallel with proliferation of gastric cancer cells. From these data, it seems that the expression of gap junction might be regulated by Wnt signaling.
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