2003 Fiscal Year Final Research Report Summary

Development of the method to select the most effective anti-cancer chemotherapy using in-house cDNA microarray

Research Project

Project/Area Number	13470426
Research Category	Grant-in-Aid for Scientific Research (B)
Allocation Type	Single-year Grants
Section	一般
Research Field	Surgical dentistry
Research Institution	Chiba University
Principal Investigator	UZAWA Katsuhiro Chiba University, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (30302558)
Co-Investigator(Kenkyū-buntansha)	SEKI Naohiko Chiba University, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (50345013) YOKOE Hidetaka Chiba University, University Hospital, Lecturer, 医学部附属病院, 講師 (70261930) TANZAWA Hideki Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (50236775)
Project Period (FY)	2001 – 2003
Keywords	DNA microarray / oral squamous cell carcinoma / chemotherapy / drug resistance
Research Abstract	The aim of the study is to analyze the mechanism involved in anticancer-drug resistance in oral squamous cell carcinoma (OSCC) and to find new molecular markers for drug resistance. H-1R cells were established in the presence of increasing concentrations of Cisplatin (CDDP) from H-1 cells in Department of Oral Surgery, Wakayama Medical University. To identify genes that might be associated with drug resistance, we used an in-house cDNA microarray representing 2,241 oral disease origin genes. H-1R exhibited 10-fold increased resistance to CDDP, compared with H-1 cells by MTT assay. The expressions of MDR genes were up-regulated in H-1R cells. The results of microarray analysis showed that 34 genes were identified to be up-regulated 2-fold or higher and 19 genes were down-regulated 2-fold or more in resistant cell, compared with parent cell. The results which were detected by the cDNA microarray were confirmed by real time PCR. Out of the up-regulated genes, the high expression of CD55 gene was commonly detected among cell lines and clinical tissue samples of OSCC. Our result suggested that the genes, especially CD55, identified to be differentially expressed in CDDP resistant cells could be new molecular markers for drug resistance.