Anti-carcinogenic actions of glycoprotein conjugated with isoflavones from submerged-liquid culture of Agaricus blazei mycelia through reciprocal expression of Bcl-2 and Bax proteins.
10.12729/jbr.2014.15.4.200
- Author:
Young Suk KIM
1
;
Boh Hyun KIM
;
Gon Sup KIM
;
Joung Soon JANG
;
So Young KIM
;
Byeong Dae CHOI
;
Jeong Ok KIM
;
Yeong Lae HA
Author Information
1. Department of Applied Chemistry, College of Agriculture and Life Science, and Institute of Agriculture and Life Science, Gyeongsang National University, Jinju 660-701, Korea. ylha@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Agaricus blazei mycelium (ABM);
apoptosis;
caspase 3;
human breast cancer MCF-7 cells;
isoflavone-conjugated glycoproteins (Gluvone)
- MeSH:
Agaricales;
Agaricus*;
Animals;
Anticarcinogenic Agents;
Apoptosis;
bcl-2-Associated X Protein*;
Bisbenzimidazole;
Breast Neoplasms;
Caspase 3;
Caspase 8;
Caspase 9;
Cell Death;
Cytochromes c;
Cytosol;
Down-Regulation;
Fruit;
Glycoproteins*;
Humans;
Isoflavones*;
MCF-7 Cells;
Mitochondria;
Molecular Weight;
Up-Regulation
- From:Journal of Biomedical Research
2014;15(4):200-206
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Glycoproteins isolated from fruit bodies and mycelial cultures of mushrooms exhibit anti-carcinogenic actions in human cancer cells and animal tumor cells by induction of apoptosis. Here, we report that isoflavone-conjugated glycoproteins (designate Gluvone), exhibit strong anti-carcinogenic effects on human breast cancer MCF-7 cells by induction of apoptosis. Gluvone with 9.4 kDa of molecular weight was isolated from submerged-liquid culture of Agaricus blazei mycelia (ABM) in soy flake-containing liquid medium. MCF-7 cells were incubated with various amounts of Gluvone (0~250 microM) for a period of 6 days. Gluvone exhibited anti-proliferative actions in a dose-dependent manner and 62% growth inhibition at 200 microM for 4 days relative to control. Hoechst 33258 staining analysis revealed that Gluvone induced formation of apoptotic bodies. Gluvone was associated with down-regulation of anti-apoptotic Bcl-2 protein expression as well as up-regulation of pro-apoptotic Bax protein expression. Gluvone treatment induced proteolytic activation of caspase-9 and caspase-3 through cytochrome c release from mitochondria to cytosol as well as concomitant degradation of poly (ADP-ribose) polymerase (PARP). In addition, Gluvone induced activation of caspase-8. Taken all together, these results indicate that the anti-proliferative effect of Gluvone is associated with induction of apoptotic cell death through the mitochondrial dysfunction pathway mediated by enhancement of Bax protein expression and suppression of Bcl-2 protein expression.
