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      A novel anti-proliferative pentapeptide (ILYMP) isolated from Cyclina sinensis protein hydrolysate induces apoptosis of DU-145 prostate cancer cells

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          Abstract

          Prostate cancer is the main causes of cancer associated mortality in men worldwide, cancer patients often suffer serious side effects when treated with chemotherapy or radiotherapy, therefore novel drugs are in high demand to treat prostate cancer. In the present study, a pentapeptide (Ile-Leu-Tyr-Met-Pro; ILYMP) with a molecular weight of 635.71 Da was isolated from the protein hydrolysate of Cyclina sinensis via ultrafiltration and chromatographic methods, and subsequently named Cyclina sinensis pentapeptide (CSP). The activity of CSP was first investigated in prostate cancer (PCa) DU-145 cells. CSP was demonstrated to significantly inhibit DU-145 cell proliferation at a half-maximal inhibitory concentration of 11.25 mM at a 72 h time interval. In addition, the results of acridine orange/ethidium bromide double staining, scanning electron microscopy and flow cytometry analyses suggested that CSP inhibited DU-145 cell proliferation via the induction of apoptosis. Following treatment with CSP, Bcl-2-associated X (Bax), cleaved caspase-3 and cleaved caspase-9 protein expression levels were enhanced in DU-145 cells; whereas B-cell lymphoma 2 expression was suppressed in DU-145 cells. In conclusion, to the best of the authors' knowledge, this is the first study to investigate the effects of an anti-proliferative peptide derived from Cyclina sinensis on DU-145 cells, and the results suggested that CSP may represent a therapeutic nutraceutical agent for the treatment of patients with PCa.

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          Abiraterone acetate for treatment of metastatic castration-resistant prostate cancer: final overall survival analysis of the COU-AA-301 randomised, double-blind, placebo-controlled phase 3 study.

          Abiraterone acetate improved overall survival in metastatic castration-resistant prostate cancer at a preplanned interim analysis of the COU-AA-301 double-blind, placebo-controlled phase 3 study. Here, we present the final analysis of the study before crossover from placebo to abiraterone acetate (after 775 of the prespecified 797 death events). Between May 8, 2008, and July 28, 2009, this study enrolled 1195 patients at 147 sites in 13 countries. Patients were eligible if they had metastatic castration-resistant prostate cancer progressing after docetaxel. Patients were stratified according to baseline Eastern Cooperative Oncology Group (ECOG) performance status, worst pain over the past 24 h on the Brief Pain Inventory-Short Form, number of previous chemotherapy regimens, and type of progression. Patients were randomly assigned (ratio 2:1) to receive either abiraterone acetate (1000 mg, once daily and orally) plus prednisone (5 mg, orally twice daily) or placebo plus prednisone with a permuted block method via an interactive web response system. The primary endpoint was overall survival, analysed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT00091442. Of the 1195 eligible patients, 797 were randomly assigned to receive abiraterone acetate plus prednisone (abiraterone group) and 398 to receive placebo plus prednisone (placebo group). At median follow-up of 20·2 months (IQR 18·4-22·1), median overall survival for the abiraterone group was longer than in the placebo group (15·8 months [95% CI 14·8-17·0] vs 11·2 months [10·4-13·1]; hazard ratio [HR] 0·74, 95% CI 0·64-0·86; p<0·0001). Median time to PSA progression (8·5 months, 95% CI 8·3-11·1, in the abiraterone group vs 6·6 months, 5·6-8·3, in the placebo group; HR 0·63, 0·52-0·78; p<0·0001), median radiologic progression-free survival (5·6 months, 5·6-6·5, vs 3·6 months, 2·9-5·5; HR 0·66, 0·58-0·76; p<0·0001), and proportion of patients who had a PSA response (235 [29·5%] of 797 patients vs 22 [5·5%] of 398; p<0·0001) were all improved in the abiraterone group compared with the placebo group. The most common grade 3-4 adverse events were fatigue (72 [9%] of 791 patients in the abiraterone group vs 41 [10%] of 394 in the placebo group), anaemia (62 [8%] vs 32 [8%]), back pain (56 [7%] vs 40 [10%]), and bone pain (51 [6%] vs 31 [8%]). This final analysis confirms that abiraterone acetate significantly prolongs overall survival in patients with metastatic castration-resistant prostate cancer who have progressed after docetaxel treatment. No new safety signals were identified with increased follow-up. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Bcl-2-family proteins and the role of mitochondria in apoptosis.

            Mitochondria are central to many forms of cell death, usually via the release of pro-apoptotic proteins from the mitochondrial intermembrane space. Some intermembrane space proteins, including cytochrome c, Smac/DIABLO, and Omi/Htra2, can induce or enhance caspase activation, whereas others, such as AIF and endonuclease G, might act in a caspase-independent manner. Intermembrane space protein release is often regulated by Bcl-2-family proteins. Recent evidence suggests that pro-apoptotic members of this family, by themselves, can permeabilize the outer mitochondrial membrane without otherwise damaging mitochondria. Mitochondria can contribute to cell death in other ways. For example, they can respond to calcium release from the endoplasmic reticulum by undergoing the mitochondrial permeability transition, which in turn causes outer membrane rupture and the release of intermembrane space proteins. Bcl-2-family proteins can influence the levels of releasable Ca(2+) in the endoplasmic reticulum, and thus determine whether the released Ca(2+) is sufficient to overload mitochondria and induce cell death.
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              Enzalutamide in castration-resistant prostate cancer patients progressing after docetaxel and abiraterone.

              Abiraterone, an androgen synthesis inhibitor, has been successfully used in the treatment of castration-resistant prostate cancer (CRPC) for 2 yr. Enzalutamide is a second-generation nonsteroidal antiandrogen that has recently been approved for the same indication. This is the first study to evaluate the effectiveness of enzalutamide after failure of abiraterone. Thirty-five patients were identified as having received sequential therapy with abiraterone followed by enzalutamide. All patients had undergone prior docetaxel chemotherapy, and no patient had received ketoconazole. Posttreatment changes in prostate-specific antigen (PSA) were used to determine the activity of enzalutamide in patients who had received prior abiraterone. The median duration of abiraterone treatment was 9.0 mo (range: 2.0-19.0 mo). Of the 35 patients, 16 (45.7%) achieved a >50% decline in PSA, and 14 (40%) had a rising PSA as the best response. The median duration of subsequent enzalutamide treatment was 4.9 mo (Kaplan-Meier estimate; 95% confidence interval [CI], 2.4-7.4). Seven of 16 CRPC patients who were initially abiraterone-sensitive (43.8%) and 3 of 19 CRPC patients who were initially abiraterone-insensitive (15.8%) showed a >50% PSA decline while taking enzalutamide. Of the 35 patients, 17 (48.6%) were primarily enzalutamide-resistant and showed a rising PSA as the best response. Median time to progression was 4.0 mo (95% CI, 2.0-6.0) for 18 of 35 patients with at least one declining PSA value while taking enzalutamide (51.4%). Of the 17 patients who were assessable radiologically, only 1 (2.9%) attained a confirmed partial response. Small sample size was the major limitation. Enzalutamide treatment achieved only a modest response rate in patients progressing after abiraterone. Although cross-resistance between abiraterone and enzalutamide was a common phenomenon, it was not inevitable, and a small but significant number of patients showed significant benefit from sequential treatment. Copyright © 2013 European Association of Urology. Published by Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                July 2018
                14 May 2018
                14 May 2018
                : 18
                : 1
                : 771-778
                Affiliations
                [1 ]School of Food and Pharmacy, Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, Zhejiang Ocean University, Zhoushan, Zhejiang 316022, P.R. China
                [2 ]Aquatic Processing Department, Zhejiang Marine Fisheries Research Institution, Zhoushan, Zhejiang 316021, P.R. China
                Author notes
                Correspondence to: Professor Zuisu Yang, School of Food and Pharmacy, Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, Zhejiang Ocean University, 1 Haida South Road, Lincheng, Changzhi Island, Zhoushan, Zhejiang 316022, P.R. China, E-mail: abc1967@ 123456126.com
                Article
                mmr-18-01-0771
                10.3892/mmr.2018.9019
                6059706
                5b07d866-f0df-4441-952f-50f8c70bb851
                Copyright: © Yu et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 24 October 2017
                : 16 April 2018
                Categories
                Articles

                cyclina sinensis,prostate cancer,protein hydrolysate,peptide,anticancer activity,apoptosis

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