Cell-cycle arrest and apoptosis induction in human breast carcinoma MCF-7 cells by carboxymethylated β-glucan from the mushroom sclerotia of Pleurotus tuber-regium

The mechanism for the anti-tumor activity of a water-soluble carboxymethylated β-glucan (CMPTR), partially synthesized from an insoluble native glucan isolated from the sclerotia of Pleurotus tuber-regium, was studied using human breast carcinoma MCF-7 breast cancer cells in vitro. CMPTR-induced ant...

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Veröffentlicht in:Carbohydrate polymers 2006-11, Vol.66 (4), p.455-462
Hauptverfasser: Zhang, Mei, Cheung, Peter C.-K., Chiu, Lawrence C.-M., Wong, Elaine Y.-L., Ooi, Vincent E.-C.
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container_end_page 462
container_issue 4
container_start_page 455
container_title Carbohydrate polymers
container_volume 66
creator Zhang, Mei
Cheung, Peter C.-K.
Chiu, Lawrence C.-M.
Wong, Elaine Y.-L.
Ooi, Vincent E.-C.
description The mechanism for the anti-tumor activity of a water-soluble carboxymethylated β-glucan (CMPTR), partially synthesized from an insoluble native glucan isolated from the sclerotia of Pleurotus tuber-regium, was studied using human breast carcinoma MCF-7 breast cancer cells in vitro. CMPTR-induced anti-proliferative activity dose-dependently, with an IC 50 of 204 μg/ml. CMPTR inhibited the cell proliferation of MCF-7 by arresting the G 1 phase of its cell cycle after 48 h of incubation as shown by flow cytometry. Such G 1 phase arrest was associated with the down-regulation of cyclin D1 and cyclin E expressions in the breast cancer cells. In addition, the CMPTR-treated MCF-7 cancer cells were associated with decreased expression of anti-apoptotic Bcl-2 protein and increased expression of Bax/Bcl-2 ratio. This study shows that CMPTR can inhibit the proliferation of MCF-7 by cell-cycle arrest and apoptosis induction. The potential development of this mushroom polysaccharide as a water-soluble anti-tumor agent requires further investigation.
doi_str_mv 10.1016/j.carbpol.2006.03.031
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CMPTR-induced anti-proliferative activity dose-dependently, with an IC 50 of 204 μg/ml. CMPTR inhibited the cell proliferation of MCF-7 by arresting the G 1 phase of its cell cycle after 48 h of incubation as shown by flow cytometry. Such G 1 phase arrest was associated with the down-regulation of cyclin D1 and cyclin E expressions in the breast cancer cells. In addition, the CMPTR-treated MCF-7 cancer cells were associated with decreased expression of anti-apoptotic Bcl-2 protein and increased expression of Bax/Bcl-2 ratio. This study shows that CMPTR can inhibit the proliferation of MCF-7 by cell-cycle arrest and apoptosis induction. 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CMPTR-induced anti-proliferative activity dose-dependently, with an IC 50 of 204 μg/ml. CMPTR inhibited the cell proliferation of MCF-7 by arresting the G 1 phase of its cell cycle after 48 h of incubation as shown by flow cytometry. Such G 1 phase arrest was associated with the down-regulation of cyclin D1 and cyclin E expressions in the breast cancer cells. In addition, the CMPTR-treated MCF-7 cancer cells were associated with decreased expression of anti-apoptotic Bcl-2 protein and increased expression of Bax/Bcl-2 ratio. This study shows that CMPTR can inhibit the proliferation of MCF-7 by cell-cycle arrest and apoptosis induction. 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source Elsevier ScienceDirect Journals
subjects Antineoplastic agents
Apoptosis
Applied sciences
Biological and medical sciences
Carboxymethylation
Cell-cycle arrest
Exact sciences and technology
General aspects
MCF-7 cells
Medical sciences
Mushroom sclerotia
Natural polymers
Pharmacology. Drug treatments
Physicochemistry of polymers
Pleurotus tuber-regium
Sclerotia
Starch and polysaccharides
β-Glucan
title Cell-cycle arrest and apoptosis induction in human breast carcinoma MCF-7 cells by carboxymethylated β-glucan from the mushroom sclerotia of Pleurotus tuber-regium
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