Bortezomib inhibits cell proliferation in prostate cancer
Author(s) -
REN-PING ZHENG,
Wei Wang,
Chuandong Wei
Publication year - 2015
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2015.2617
Subject(s) - du145 , bortezomib , cell cycle , apoptosis , cell growth , cancer research , prostate cancer , cancer cell , cell , mtt assay , flow cytometry , chemistry , cancer , biology , pharmacology , medicine , microbiology and biotechnology , immunology , multiple myeloma , biochemistry , lncap
Despite the improvement in chemotherapeutic agents, the outcome of patients with prostate cancer remains poor. It is therefore imperative that new anticancer drugs are explored. The aim of the present study was to investigate the inhibitory effect of bortezomib on DU145 prostate cancer cells. The DU145 cell proliferation rate was detected via MTT assay prior to and following exposure to various concentrations of bortezomib, and the level of cell apoptosis and the cell cycle distribution were tested using flow cytometry. In addition, western blotting was used to measure the expression of Bcl-2-interacting killer (Bik) and active-caspase-3. The results showed that bortezomib inhibited the proliferation of DU145 cells in a time- and dose-dependent manner. Following treatment with 1.6 µmol/l bortezomib, the DU145 cells showed marked nuclear condensation, chromatin condensation and fragmentation. Analysis of the cell cycle revealed a significantly increased percentage of cells in the G0/G1 phase and a decreased percentage in the S and G2/M phases. The rate of DU145 cell apoptosis was significantly higher in the bortezomib group than that in the control group, and this was accompanied by an enhanced expression of Bik and active-caspase-3. It can be concluded that bortezomib inhibits the proliferation of DU145 cells by inducing apoptosis. The underlying mechanism may involve the upregulation of Bik and active-caspase-3 expression.
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