Characterization and gene profiling in oral cancer cells chronic exposured to areca nut extract

• Main Authors: Chi Tung Lin, 林紀東
• Other Authors: A. J. Cheng
• Format: Others
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/asn5kk

碩士 === 長庚大學 === 醫學生物技術研究所 === 96 === Oral cancer is one of the major malignant tumors in Taiwan. Areca nut chewing is the major risk factor associated with this disease, however, the molecular mechanisms leading to oral carcinogenesis is unclear. Aim of this study is to characterize the potential phenotype alteration and global survey of the gene expression profile in oral cancer cells subjected to chronic exposure of areca nut extract (ANE). Two oral cancer cell lines OECM1 and SAS were used. After periodically treatment (24 hours per passage) of the cells with IC70 dose of ANE for 100 days, the chronic treatment sublines have been established. These sublines have been found suppressed in growth (38% and 57% reduction at day 3), reduced in colony formation (~50% and 40%), and cell migration ability. Resistance to DNA-damaged stress and increased ROS scavenge ability were also found in the ANE-trained sublines. cDNA microarray analyses were applied to global survey the gene expression alterations in ANE-trained sbulines. Total of 174 and 51 genes were found 2-fold differential expressed respectively in OECM1 and SAS sbulines, which participated in several cell regulatory pathways including metabolites, cell adhesion / mobility, homeostasis, immunity, and signal transduction. These data set of networks provide a base and direction for further studies. Nine genes were found differentially expressed in both sublines, and 6 were further validated by RT-PCR assay. In which, HMGS1 and KRT-17 were up-regulation whereas ID-1, IRA-1, CEMPF and SMC-4 were down regulation in both ANE chronic treatment cells. These results indicate that these genes may play roles leading to phenotype alteration and eventually oral carcinogenesis. The underlined mechanism will be further investigated.