We focused the characterization of BI-1 as a cancer metastasis protein.
We are accumulating the evidences of the theory: BI-1-induced cancer metastasis,
① BI-1-induced extracellular acidity is related with sodium-hydrogen exchanger activation
② The interaction of BI-1 with actin induces cancer cell adhesion through actin polymerization enhancement
③ BI-1-induced Ca2+/H+ antiporter activation is one of BI-1 endogenous function.
We screened the chemicals to regulate acidic environments in BI-1-overexpressing cells. In the presence of the chemicals, mitochondria function can be affected in BI-1-overexpressing cells: This is our hypothesis. Under the hypothesis, we searched the chemicals which are regulating the BI-1-induced mitochondrial alteration. We found the potential candidates including doxorubicin through the regulation screening of Rieske-FeS, a component of mitochondrial complex III. As a plan for this study, the basic studies will be in-depth established. To understand what BI-1 has functions in clinical situation, we plan to obtain the expression of BI-1-related data in cancer patient samples. In addition, we plan to integrate the basic role of BI-1 into clinical meanings.