Blocks of cell communication and apoptosis in carcinogenesis

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Research aim of this project is to focus on possible interacting mechanism between two independent phenotypes during the course of epigenetic carcinogenesis, i.e., block of the gap junction intercellular communication (GJIC) and the inhibition of apoptosis.Main body of accomplishment of the research is to have found a link of GSH along the MAP kinase signal transduction between the block of GJIC and the induction of apoptosis after treatment of an epigenetic carcinogenic chemical, H_2O_2. The results were sent to a journal for consideration of possible publication.In addition to above, further following progress facilitating these research area was made : First, as an in vitro system hepatic cell line, WB-myc cell, carrying v-myc gene was established from rat, which is potent powerful system to induce experimental apoptosis by penta-chloro-phenol, an epigenetic carcinogenic model compound, second, as an in vivo system, a facilitation of research on GJIC under apoptosis in p53-deficient mice, third, another in vivo system, a facilitation of apoptosis study in various connexin deficiency mice, such as connexin(Cx) 32 knockout(KO), Cx43-KO.