Chios Gum Mastic Induces Cell Cycle Arrest and Apoptosis in Human Osteosarcoma Cells.
- Author:
Ji Hak MIN
1
;
Do Kyun KIM
;
Hyun Ho KWAK
;
Gyoo Cheon KIM
;
Seung Eun LEE
;
In Ryoung KIM
;
Chul Hoon KIM
;
Bong Soo PARK
Author Information
1. Department of Oral Anatomy, School of Dentistry, Pusan National University, Yangsan, Korea. parkbs@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Chios gum mastic (CGM);
Apoptosis;
Cell cycle arrest;
Human osteosarcoma cells (HOS cells)
- MeSH:
Apoptosis;
Blotting, Western;
Cell Cycle;
Cell Cycle Checkpoints;
Cell Death;
Cell Survival;
Dietary Supplements;
DNA;
Duodenal Ulcer;
Electrophoresis;
Flow Cytometry;
G1 Phase Cell Cycle Checkpoints;
Gingiva;
Greece;
Humans;
Immunohistochemistry;
In Situ Nick-End Labeling;
Medicine, Traditional;
Membrane Potential, Mitochondrial;
Microscopy, Confocal;
Osteosarcoma;
Plants;
Proteasome Endopeptidase Complex;
Proteins;
Resins, Plant;
Stomach
- From:Korean Journal of Anatomy
2009;42(4):245-256
- CountryRepublic of Korea
- Language:English
-
Abstract:
Chios gum mastic (CGM) is a resin produced from the stem and leaves of Pistiacia lentiscus L var chia, a plant which grows only on Chios Island in Greece. CGM has been used for many centuries as a dietary supplement and folk medicine for stomach and duodenal ulcers in many Mediterranean countries and is also known to induce cell cycle arrest and apoptosis in some cancer cells. This study was undertaken to investigate the alteration of the cell cycle and induction of apoptosis by CGM treatment on human osteosarcoma (HOS) cells. The viability and the growth inhibition of HOS cells were assessed by the MTT assay and clonogenic assay respectively. The hoechst staining, TUNEL assay and DNA electrophoresis were conducted to observe the HOS cells undergoing apoptosis. HOS cells were treated with CGM, and Western blotting, immunocytochemistry, confocal microscopy, FACScan flow cytometry, mitochondrial membrane potential change and proteasome activity were conducted. CGM treatment of HOS cells was found to result in a dose- and time-dependent decrease in cell viability, a dose-dependent inhibition of cell growth, and apoptotic cell death. Tested HOS cells also showed several lines of apoptotic manifestation and G1 arrest in cell cycle progression. In summary, this study clearly demonstrated that CGM induces G1 cell cycle arrest via the modulation of cell cycle-related proteins, and apoptosis via proteasome, mitochondrial and caspase cascades in HOS cells. Therefore, our data provide the possibility that a natural product, CGM could be considered as a novel therapeutic strategy for human osteosarcoma.
