Earlier the authors demonstrated that the process of
tumor progression in vivo may be inhibited or accelerated depending on the conditions of
tumor growth (accelerated by
tumor cell dissemination or delayed in locally growing
tumors). It was also shown that
tumor progression is inhibited in case of bcl-2 gene transduction in
tumor cells. In this study, the research into mechanisms of the acceleration or inhibition of
tumor progression and the role that Bcl-2 family
proteins may play in these phenomena was continued. The results of the study demonstrated the following 1) immediate in vivo activation of endogenous proapoptotic
Bax protein in disseminated
tumor cells, not protected by Bcl-2 against apoptosis, and its correlation with accelerated
tumor progression; 2) complete suppression of in vivo Bax activation in
tumor cells protected by Bcl-expression, and inhibited
tumor progression; 3) alternative character of Bcl-2 and Bax expression under the conditions of accelerated and inhibited
tumor progression. Thus, the data presented support the hypothesis that the rates of
tumor progression in vivo are regulated depending on the initial anti- and proapoptotic programs of
tumor cells.