Key roles of BIM-driven apoptosis in epithelial tumors and rational chemotherapy.
作者： Ting-Ting Tan , Kurt Degenhardt , Deirdre A. Nelson , Brian Beaudoin , Wilberto Nieves-Neira
DOI: 10.1016/J.CCR.2005.02.008
关键词:
摘要: Defective apoptosis not only promotes tumorigenesis, but also can confound chemotherapeutic response. Here we demonstrate that the proapoptotic BH3-only protein BIM is a tumor suppressor in epithelial solid tumors and determinant paclitaxel sensitivity vivo. Furthermore, H-ras/mitogen-activated kinase (MAPK) pathway conferred resistance to was dependent on functional inactivation of BIM. Whereas induced accumulation BIM-dependent vitro vivo, H-ras/MAPK suppressed this induction by phosphorylating targeting for degradation proteasomes. The proteasome inhibitor Velcade (P-341, Bortezomib) restored induction, abrogated H-ras-dependent resistance, promoted regression, suggesting potential benefits combinatorial chemotherapy paclitaxel.
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