J Biomed Res.
2014 Dec;15(4):200-206. 10.12729/jbr.2014.15.4.200.
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
- Affiliations
-
- 1Department 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
- 2Laboratory of Biochemistry, School of Veterinary Medicine, Gyeongsang National University, Jinju 660-701, Korea.
- 3Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul 156-576, Korea.
- 4Department of Food and Nutrition, International University of Korea, Jinju 660-759, Korea.
- 5Department of Marine Food and Life Science Engineering, College of Marine Science, Gyeongsang National University, Tongyoung 650-160, Korea.
- 6HK Biotech, Co. Ltd., Jinju 660-844, Korea.
- KMID: 2169000
- DOI: http://doi.org/10.12729/jbr.2014.15.4.200
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.
Keyword
MeSH Terms
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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
Anticarcinogenic Agents
Bisbenzimidazole
Caspase 3
Caspase 8
Caspase 9
Cytochromes c
Glycoproteins
Isoflavones
bcl-2-Associated X Protein
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