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The proteasome inhibitor, bortezomib, induces prostate cancer cell death by suppressing the expression of prostate-specific membrane antigen, as well as androgen receptor.
Abstract The progression of primary prostate cancer (PC) is dependent on the androgen receptor (AR) and prostate‑specific membrane antigen (PSMA). Furthermore, the growth of PC cells is terminated with the downregulation of both AR and PSMA. In our preliminary experiments, it was also found that bortezomib (BZ; PS‑341) that inhibits 26S proteasome activity, acts as a downregulator of both PSMA and AR. In addition to evaluating the effects of BZ on protein expression, the present study evaluated and compared the anticancer effects of BZ on the growth of cells treated with BZ, docetaxel (DOC), or a combinatio...
Source: International Journal of Oncology - February 1, 2019 Category: Cancer & Oncology Authors: Kuroda K, Liu H Tags: Int J Oncol Source Type: research

Bortezomib induces apoptosis and suppresses cell growth and metastasis by inactivation of Stat3 signaling in chondrosarcoma.
Abstract Bortezomib, formerly known as PS341, is a novel proteasome inhibitor with in vitro and in vivo antineoplastic effects in many malignancies. However, diverse antitumor mechanisms of bortezomib have been identified in many investigations and preclinical studies. Understanding the molecular and cellular mechanisms through which bortezomib acts will improve the therapeutic utility of this drug in different cancer types. In the present study, we investigated the in vitro and in vivo effects of bortezomib on chondrosarcoma. Bortezomib selectively inhibited cell growth in chondrosarcoma cells but not in norma...
Source: International Journal of Oncology - December 13, 2016 Category: Cancer & Oncology Authors: Bao X, Ren T, Huang Y, Ren C, Yang K, Zhang H, Guo W Tags: Int J Oncol Source Type: research

Proteasome inhibitor-resistant cells cause EMT-induction via suppression of E-cadherin by miR-200 and ZEB1.
Abstract Downregulation of E-cadherin (gene: CDH1) plays an important role in epithelial-mesenchymal transition (EMT), which is critical for normal development and disease states. As a result of long-term treatment of endometrial carcinoma Ishikawa cells with epoxomicin (EXM), the cells exhibited the phenotype for EXM-resistance (Ish/EXM cells). Moreover, CDH1 mRNA and its protein were suppressed and EMT was induced in Ish/EXM cells. Ish/EXM cells exhibited drug-resistance to other proteasome inhibitors, MG-132, PSI and PS-341 (Bortezomib). The proteasome inhibitor-resistant cells acquired invasiveness as a result...
Source: International Journal of Oncology - March 4, 2015 Category: Cancer & Oncology Authors: Asakura T, Yamaguchi N, Ohkawa K, Yoshida K Tags: Int J Oncol Source Type: research