Bcl-2 and Bcl-xl counteract the proapoptotic effects of Bax and Bcl-2 antagonist find more killer and inhibit the mitochondria-mediated cell death pathway [38]. Once the expression of Bcl-2 and/or Bcl-xl decreases, elevated Bax translocates to the mitochondria membrane, induces the opening of the mitochondrial permeability transition pore (PTP) to release Cytochrome C and causes mitochondria-dependent apoptosis. Here, we showed that Ad-bFGF-siRNA antagonizes the STAT3 pathway activation
and depolarizes membrane potentials to induce depolarization of mitochondria and apoptosis in U251 cells. In conclusion, as one of the new avenues in gene therapy, siRNA has emerged as a great potential for the treatment of glioma. The adenovirus-mediated delivery of bFGF siRNA presents one such promising approach and the current data provide a mechanistic explanation for this novel strategy. Future studies
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