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.

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