| Literature DB >> 12424198 |
Nicholas Mitsiades1, Constantine S Mitsiades, Paul G Richardson, Vassiliki Poulaki, Yu-Tzu Tai, Dharminder Chauhan, Galinos Fanourakis, Xuesong Gu, Charles Bailey, Marie Joseph, Towia A Libermann, Robert Schlossman, Nikhil C Munshi, Teru Hideshima, Kenneth C Anderson.
Abstract
The proteasome inhibitor PS-341 inhibits nuclear factor-kappaB (NF-kappaB) activation, induces apoptosis in cancer cells, including multiple myeloma (MM) cells, and has marked clinical activity as a monotherapy for MM. In this study, we found that subtoxic concentrations of PS-341 potently sensitized MM cell lines and patient cells to DNA-damaging chemotherapeutic agents such as doxorubicin and melphalan, including cells resistant to these drugs and those isolated from a patient who had relapsed after PS-341 monotherapy. Moreover, PS-341 abolished cell adhesion-mediated drug resistance. Using gene expression profiling and proteomic analysis, we demonstrate that PS-341, among its other proapoptotic effects, down-regulates the expression of several effectors involved in the cellular response to genotoxic stress. These data suggest that, in addition to down-regulating the expression of apoptosis inhibitors, PS-341 inhibits genotoxic stress response pathways and thereby restores sensitivity to DNA-damaging chemotherapeutic agents. These studies, therefore, provide the framework for clinical use of this agent in combination with conventional chemotherapy.Entities:
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Year: 2002 PMID: 12424198 DOI: 10.1182/blood-2002-06-1768
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113