철 킬레이터 처리한 구강 불멸화 및 악성 각화세포에서 유전자 발현 Profiling

서지정보

ㆍ발행기관 : 대한구강악안면병리학회 ㆍ수록지정보 : 대한구강악안면병리학회지 / 32권 / 4호
ㆍ저자명 : 이선경, 이화정, 이상임, 김선주, 김영숙, 이영만, 우상형, 김민관, 박제상, 이화준, 이승훈, 이준, 김은철

목차

I. 서론
II. 연구 재료 및 방법
1. 세포배양
2. cDNA microarray
3. microarray 실험
4. data 분석
III. 결과
IV. 고찰
V. 결론
VI. 참고문헌

영어 초록

Considering the great potential of iron chelators at inhibiting the proliferation of tumor cells, in order to determine the molecular and biological basis for the effects of iron chelator in oral cancer, we investigated the effects of iron chelator, desferrioxamine (DFO), on the gene profiling analysis of immortalized human oral keratinocytes (IHOK), and oral cancer cells (HN12), using the cDNA microarray. We identified 46 clones cDNA exhibiting more than 2 fold overexpression in DFO treated IHOK and HN12 cells, and 94 cDNA reveal more than 2 fold down-regulated expression. Examination of gene expression that differs between DFO treated vs. control IHOK and HN12 cells apprear to be related to : cell cycle regulator, cell growth and apoptosis, signal transduction and stress. p21 for cell cell cycle factor was upregualted, and cyclin-cdk gene was decreased expression, so we observed cell cycle arrest in DFO treated IHOK and HN12 cells. In tumor growth, we have identified downregulation of hemidesmosomal protein (bullous pemphigoid antigen 1) and epiregulin expression in DFO treated IHOK and oral cancer cells. Signal transducers including mitogen-activated protein kinase-activated protein kinase 5, serine/thereonine kinase 6 were downregulated with DFO treated cells, suggesting the DFO regulates the p38 MAP kianse pathway in immortalized and maignant oral keratincytes. In conclusion, we have demonstrated the high-throughput utility of cDNA array hybridization in parallel to the gene expression analysis to identify genes that are expressed differentially in DFO treated with immortalized and malignant oral keratinocytes. The differentially expressed genes identified here should be informative in DFO-induced anti-cancer effects.

참고 자료

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