Publication:
α-Mangostin induces apoptosis in human chondrosarcoma cells through downregulation of ERK/JNK and Akt signaling pathway

2
0

Issued Date

2011

Resource Type

Article

File Type

application/pdf

ISSN

218561

DOI

10.1021/jf200620n

Other identifier(s)

2-s2.0-79957964309

Rights Holder(s)

Scopus

Bibliographic Citation

Journal of Agricultural and Food Chemistry. Vol 59, No.10 (2011), p.5746-5754

Suggested Citation

Krajarng A., Nakamura Y., Suksamrarn S., Watanapokasin R. α-Mangostin induces apoptosis in human chondrosarcoma cells through downregulation of ERK/JNK and Akt signaling pathway. Journal of Agricultural and Food Chemistry. Vol 59, No.10 (2011), p.5746-5754. doi:10.1021/jf200620n Retrieved from: https://hdl.handle.net/20.500.14740/7328

Title

α-Mangostin induces apoptosis in human chondrosarcoma cells through downregulation of ERK/JNK and Akt signaling pathway

Author(s)

Krajarng A.
 Nakamura Y.
 Suksamrarn S.
 Watanapokasin R.

Abstract

Chondrosarcoma is a malignant primary bone tumor that is resistant to chemotherapy and radiation therapy. α-Mangostin, a component of Garcinia mangostana Linn, is a xanthone derivative shown to have antioxidant and antitumor properties. This study is the first to investigate anticancer effects of α-mangostin in the human chondrosarcoma cell line SW1353. We showed that α-mangostin inhibited cell proliferation of SW1353 cells in a time-and dose-dependent manner by using the trypan blue exclusion method. Hoechst 33342 nuclear staining and nucleosomal DNA-gel electrophoresis revealed that α-mangostin could induce nuclear condensation and fragmentation, typically seen in apoptosis. Flow cytometry using Annexin V/PI double staining assessed apoptosis, necrosis and viability. α-Mangostin activated caspase-3,-8,-9 expression, decreased Bcl-2 and increased Bax. This promotes mitochondrial dysfunction, leading to the release of cytochrome c from the mitochondria to the cytoplasm. In addition, total and phosphorylated ERK and JNK were downregulated in α-mangostin-treated SW1353 cells but no changes in p38. α-Mangostin also decreased phosphorylated Akt without altering total Akt. These results suggest that R-mangostin inhinbited cell proliferation and induced apoptosis through downregulation of ERK, JNK and Akt signaling pathway in human chondrosarcoma SW1353 cells. © 2011 American Chemical Society.

Subject(s)

Akt
 Annexins
 Anticancer effects
 Antitumor property
 Apoptosis
 Apotosis
 Caspase-3
 Chondrosarcoma
 Chondrosarcoma cells
 Cytochrome C
 Dose-dependent manner
 Down-regulation
 Hoechst
 Induced apoptosis
 MAPK
 Mitochondrial dysfunction
 Primary bone tumors
 Radiation therapy
 Signaling pathways
 Cell culture
 Cell proliferation
 Chemotherapy
 Drug products
 Electrophoresis
 Flow cytometry
 Mitochondria
 Phosphorylation
 Signaling
 Cell death
 Antineoplastic agent
 Mangostin
 Mitogen activated protein kinase
 Protein kinase B
 Stress activated protein kinase
 Xanthone derivative
 Apoptosis
 Article
 Bone tumor
 Cell proliferation
 Chondrosarcoma
 Drug effect
 Human
 Metabolism
 Pathology
 Phosphorylation
 Signal transduction
 Tumor cell line
 Antineoplastic Agents, Phytogenic
 Apoptosis
 Bone Neoplasms
 Cell Line, Tumor
 Cell Proliferation
 Chondrosarcoma
 Extracellular Signal-Regulated MAP Kinases
 Humans
 JNK Mitogen-Activated Protein Kinases
 Mitogen-Activated Protein Kinases
 Phosphorylation
 Proto-Oncogene Proteins c-akt
 Signal Transduction
 Xanthones
 Garcinia mangostana

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URI

https://hdl.handle.net/20.500.14740/7328

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