Zhang Chun-ye, Zhou Xiao-jian, Zhang Zhi-yuan, Li Jiang
Department of Oral Pathology, School of Stomatology, Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, China.
Zhonghua Kou Qiang Yi Xue Za Zhi. 2007 Mar;42(3):135-9.
To investigate the promoter methylation status of tumor suppressor gene and the relationship between promoter methylation and mRNA, protein expression of tumor suppressor gene in salivary adenoid cystic carcinoma (ACC) cell lines.
Promoter methylation status of E-cad, p16, RASSF1A, DAPK, and MGMT was determined by methylation-specific polymerase chain reaction (MSP) in ACC cell lines, ACC-2, ACC-3, and ACC-M. E-cad, p16 protein and mRNA expression was also examined by IHC and RT-PCR in 3 ACC cell lines.
All the three salivary ACC cell lines exhibited E-cad, p16 promoter methylation, but no methylation of RASSF1A, DAPK, and MGMT was found. There was p16 protein and mRNA expression but no E-cad expression in 3 ACC cell lines.
The results suggest that in ACC cell lines, promoter methylation of E-cad, p16 is a common event, and promoter methylation may be one of the major mechanism for inactivation of E-cad.
探讨涎腺腺样囊性癌（ACC）细胞系中抑癌基因启动子甲基化状态及其与抑癌基因mRNA、蛋白表达的关系。
采用甲基化特异性聚合酶链反应（MSP）检测ACC细胞系ACC-2、ACC-3和ACC-M中E-cad、p16、RASSF1A、DAPK及MGMT的启动子甲基化状态。采用免疫组化（IHC）和逆转录-聚合酶链反应（RT-PCR）检测3种ACC细胞系中E-cad、p16蛋白及mRNA表达。
3种涎腺ACC细胞系均存在E-cad、p16启动子甲基化，未发现RASSF1A、DAPK及MGMT甲基化。3种ACC细胞系均有p16蛋白及mRNA表达，但无E-cad表达。
结果提示，在ACC细胞系中，E-cad、p16启动子甲基化是常见事件，启动子甲基化可能是E-cad失活的主要机制之一。
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