Publication: Effects of α-mangostin on apoptosis induction of human colon cancer
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Issued Date
2011
Resource Type
File Type
application/pdf
ISSN
10079327
Other identifier(s)
2-s2.0-79955932364
Rights Holder(s)
มหาวิทยาลัยศรีนครินทรวิโรฒ
Bibliographic Citation
World Journal of Gastroenterology. Vol 17, No.16 (2011), p.2086-2095
Suggested Citation
Watanapokasin R., Jarinthanan F., Nakamura Y., Sawasjirakij N., Jaratrungtawee A., Suksamrarn S. Effects of α-mangostin on apoptosis induction of human colon cancer. World Journal of Gastroenterology. Vol 17, No.16 (2011), p.2086-2095. doi:10.3748/wjg.v17.i16.2086 Retrieved from: https://hdl.handle.net/20.500.14740/7340
Abstract
AIM: To investigate the effect of α-mangostin on the growth and apoptosis induction of human colon cancer cells. METHODS: The three colorectal adenocarcinoma cell lines tested (COLO 205, MIP-101 and SW 620) were treated with α-mangostin to determine the effect on cell proliferation by MTT assay, cell morphology, chro-matin condensation, cell cycle analysis, DNA fragmentation, phosphatidylserine exposure and changing ofmitochondrial membrane potential. The molecular mechanisms of α-mangostin mediated apoptosis were further investigated by Western blotting analysis including activation of caspase cascade, cytochrome c release, Bax, Bid, p53 and Bcl-2 modifying factor.RESULTS: The highest inhibitory effect of α-mangostin on cell proliferation of COLO 205, MIP-101 and SW 620 were 9.74 ± 0.85 μg/mL, 11.35 ± 1.12 μg/mL and 19.6 ± 1.53 μg/mL, respectively. Further study showed that α-mangostin induced apoptotic cell death in COLO 205 cells as indicated by membrane blebbing, chromatin condensation, DNA fragmentation, cell cycle analysis, sub-G1 peak (P < 0.05) and phosphatidylserine exposure. The executioner caspase, caspase-3, the initiator caspase, caspase-8, and caspase-9 were expressed upon treatment with α-mangostin. Further studies of apoptotic proteins were determined by Western blotting analysis showing increased mitochondrial cytochrome c release, Bax, p53 and Bmf as well as reduced mito-chondrial membrane potential (P < 0.05). In addition, up-regulation of tBid and Fas were evident upon treatment with α-mangostin (P < 0.01).CONCLUSION: α-Mangostin may be effective as an anti-cancer agent that induced apoptotic cell death in COLO 205 via a link between extrinsic and intrinsic pathways. © 2011 Baishideng. All rights reserved.
Subject(s)
Alpha mangostin
Antineoplastic agent
Caspase
Caspase 3
Caspase 8
Caspase 9
Cell protein
Cytochrome c
Fas antigen
Garcinia mangostana extract
Initiator caspase
Phosphatidylserine
Plant extract
Protein Bax
Protein bcl 2
Protein Bid
Protein Bmf
Protein p53
Unclassified drug
Antineoplastic activity
Apoptosis
Article
Cancer cell culture
Cancer growth
Cell assay
Cell cycle
Cell death
Cell proliferation
Cell structure
Chromatin condensation
Colon cancer
Controlled study
DNA fragmentation
Drug efficacy
Drug isolation
Drug mechanism
Enzyme activation
Garcinia mangostana
Human
Human cell
Mitochondrial membrane potential
Protein expression
Protein induction
Protein secretion
Western blotting
Apoptosis
Caspases
Cell Cycle
Cell Line, Tumor
Cell Survival
Colonic Neoplasms
Cytochromes c
DNA Fragmentation
Enzyme Activation
Humans
Protein Kinase Inhibitors
Xanthones
Antineoplastic agent
Caspase
Caspase 3
Caspase 8
Caspase 9
Cell protein
Cytochrome c
Fas antigen
Garcinia mangostana extract
Initiator caspase
Phosphatidylserine
Plant extract
Protein Bax
Protein bcl 2
Protein Bid
Protein Bmf
Protein p53
Unclassified drug
Antineoplastic activity
Apoptosis
Article
Cancer cell culture
Cancer growth
Cell assay
Cell cycle
Cell death
Cell proliferation
Cell structure
Chromatin condensation
Colon cancer
Controlled study
DNA fragmentation
Drug efficacy
Drug isolation
Drug mechanism
Enzyme activation
Garcinia mangostana
Human
Human cell
Mitochondrial membrane potential
Protein expression
Protein induction
Protein secretion
Western blotting
Apoptosis
Caspases
Cell Cycle
Cell Line, Tumor
Cell Survival
Colonic Neoplasms
Cytochromes c
DNA Fragmentation
Enzyme Activation
Humans
Protein Kinase Inhibitors
Xanthones
