Mechanism of Apoptosis Induced by Ginkgo Biloba Extract(Egb 761) in Oral Cavity Cancer Cell Lines.
- Author:
Jung Hyun CHANG
1
;
Joo Heon YOON
;
Eun Chang CHOI
;
Kun Wayn LEE
;
Chang Il CHO
;
Kyung Su KIM
Author Information
1. Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea. ydrhinol@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Mouth neoplasms;
Ginkgo biloba;
Apoptosis
- MeSH:
Apoptosis*;
Blotting, Western;
Cell Line*;
Cell Proliferation;
Cyclic AMP Response Element-Binding Protein;
Ginkgo biloba*;
Hand;
Inflammation;
Mouth Neoplasms;
Mouth*;
Phosphorylation;
Phosphotransferases;
Protein Kinases;
Signal Transduction;
Transfection
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2006;49(12):1181-1187
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: According to our previous study Ginkgo biloba extract (EGb 761) induces inhibition of cell proliferation and apoptosis in SCC 1483 oral cavity cancer cells. On the other hand, in lipopolysaccharide-stimulated RAW 264.7 cells, activation of mitogen activated protein kinase (MAPK) is the key event in the inhibition of inflammation by EGb 761. Therefore, we have investigated whether MAPK pathway is involved in the apoptotic process by EGb 761 in oral cavity cancer cell lines or not. SUBJECTS AND METHOD: In SCC 1483 oral cavity cancer cell lines, Western blot analysis, Fluorescence-activated cell sorter (FACS) analysis, and transient transfection using MAPK-dominant negative constructs were used. RESULTS: When SCC 1483 oral cavity cancer cell lines were treated with the concentration of 250 microgram/ml EGb 761, activation of extracellular signal-regulated kinase (ERK) and apoptosis were noted. This apoptosis was inhibited by the treatment with ERK inhibitor (PD 98059). In the transiently transfected cells by MAPK/ERK kinase 1 (MEK1)-dominant negative construct, phosphorylations of ERK and p90 ribosomal S 6 protein kinase (RSK1) were inhibited which led to the inhibition of apoptosis by EGb 761. The inhibition of apoptosis was also noted in the transfected cells by RSK1 dominant negative construct and cAMP response element binding protein (CREB)-dominant negative construct. CONCLUSION: In conclusion, the apoptosis of SCC 1483 oral cavity cancer cell lines by EGb 761 is linked to the activation of ERK and it can happen via ERK MAPK/RSK1/CREB signal transduction pathway.
