Korean J Phys Anthropol.
2008 Mar;21(1):55-68.
Chios Gum Mastic Induces Cell Cycle Arrest and Apoptosis in YD9 Human Oral Squamous Carcinoma Cells
- Affiliations
-
- 1Department of Oral Anatomy, School of Dentistry, Pusan National University, Korea. parkbs@pusan.ac.kr
- 2Department of Oral Microbiology, School of Dentistry, Pusan National University, Korea.
- 3Department of Oral Pathology, School of Dentistry, Pusan National University, Korea.
- 4Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National University, Korea.
- 5Hyowon Dental research, Korea.
- 6Department of Oral and Maxillofacial Surgery, College of Medicine, Dong-A University Medical Center, Korea.
Abstract
- Chios gum mastic (CGM) is obtained from the stem and leaves of Pistacia lentiscus trees and has been extensively used for centuries in Mediterranean and Middle Eastern countries, both as a dietary supplement and herbal remedy. This study was undertaken to examine in vitro effects of cytotoxicity and growth inhibition, and the molecular mechanism underlying modulation of cell cycle and induction of apoptosis in YD9 human oral squamous carcinoma cell line treated with CGM. The viability of YD9 cells and human normal keratinocyes (HaCaT cells), and the growth inhibition of YD9 cells were assessed by the MTT assay and clonogenic assay respectively. The hoechst staining and DNA electrophoresis were conducted to observe the YD9 cells undergoing apoptosis. YD9 cells were treated with CGM, and Western blotting, immunocytochemistry, confocal microscopy and FACScan flow cytometry were conducted. Mitochondrial membrane potential change and proteasome activity were measured. CGM treatment on YD9 cells resulted in a does-dependent inhibition of cell growth and induced apoptotic cell death. And tested YD9 cells showed several lines of apoptotic manifestation. Flow cytometric analysis revealed that CGM resulted in G1 arrest in cell cycle progression which was associated with decrease in the protein expression of cyclin D1, cyclin D3, Cdk2 and Cdk4, and increase in the protein expression of p21(WAF1/CIP1) and p53. These results demonstrate that CGM induces G1 the cell cycle arrest via the modulation of cell cycle-related proteins, and apoptosis via mitochondria and caspase pathway in YD9 cells, suggesting that CGM can be considered as a novel therapeutic strategy for human oral squamous cell carcinoma from its strong cell cycle arrest and apoptosis-inducing activity.
Keyword
MeSH Terms
-
Apoptosis
Blotting, Western
Carcinoma, Squamous Cell
Cell Cycle
Cell Cycle Checkpoints
Cell Death
Cell Line
Cyclin D1
Cyclin D3
Dietary Supplements
DNA
Electrophoresis
Flow Cytometry
Gingiva
Humans
Immunohistochemistry
Membrane Potential, Mitochondrial
Microscopy, Confocal
Mitochondria
Pistacia
Proteasome Endopeptidase Complex
Proteins
Resins, Plant
Trees
Cyclin D1
Cyclin D3
DNA
Proteasome Endopeptidase Complex
Proteins
Resins, Plant
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