Zhang Jing, Ye Feng, Chen Huai-zeng, Ye Da-feng, Lu Wei-guo, Xie Xing
Department of Gynecologic Oncology, Women's Hospital, Medical College of Zhejiang University, Hangzhou 310006, China.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2006 Apr;28(2):173-7.
To investigate the expression of OPCML gene in ovarian epithelial carcinoma and determine the relationship between mRNA expression and methylation of their promoters.
Twenty normal ovarian tissues and 89 ovarian epithelial tumor specimens (72 malignant, 17 benign), as well as 3 ovarian carcinoma cell lines (SKOV-3, CAOV3, and 3AO), were collected for detection of OPCML gene expression by reverse transcription-polymerase chain reaction and for detection of promoter methylation by restriction enzyme cut analysis from 7. 1999 to 7. 2003.
Among ovarian epithelial carcinoma 19.4% expressed OPCML mRNA, while 85% of normal ovarian tissue and 76.5% of benign ovarian tumor. The ratio of expression of OPCML mRNA in ovarian epithelial carcinoma was significantly lower than those of normal (chi2 = 30.108, P = 0.0000) and benign tumors (chi2 = 21.162, P = 0.000). No OPCML mRNA expression was found in SKOV-3 and CAOV3, but was found in 3AO. Methylations were detected in 44.4% of cancer cells promoter, while 0% in normal ovarian tissue and benign ovarian tumors. The ratio of methylation of ovarian epithelial carcinoma was significantly higher than those of normal (chi2 = 13.630, P = 0.0000) and benign tumors (chi2 = 11.797, P = 0.000). Methylation was found in SKOV-3 and CAOV3, but not in 3AO. The relationship between gene expression and promoter methylation was correlated (r = 11.589, P = 0.002), especially at Hap I1 site (r = 11.640, P = 0.004). Methylation was also found in SKOV-3 and CAOV3 cell lines, but not in 3AO cell line.
Deletion of OPCML gene exists in ovarian epithelial carcinoma cell. The gene promoter methylations, especially Hap II motif, may be one of pathways that contribute the inhibition of OPCML expression.
研究卵巢上皮癌中OPCML基因的表达情况，并确定其mRNA表达与启动子甲基化之间的关系。
收集20例正常卵巢组织、89例卵巢上皮肿瘤标本（72例恶性、17例良性）以及3种卵巢癌细胞系（SKOV-3、CAOV3和3AO），于1999年7月至2003年7月采用逆转录聚合酶链反应检测OPCML基因表达，采用酶切分析检测启动子甲基化。
卵巢上皮癌中19.4%表达OPCML mRNA，而正常卵巢组织为85%，良性卵巢肿瘤为76.5%。卵巢上皮癌中OPCML mRNA的表达率显著低于正常组织（χ2 = 30.108，P = 0.0000）和良性肿瘤（χ2 = 21.162，P = 0.000）。SKOV-3和CAOV3中未检测到OPCML mRNA表达，但在3AO中检测到。44.4%的癌细胞启动子存在甲基化，而正常卵巢组织和良性卵巢肿瘤中为0%。卵巢上皮癌的甲基化率显著高于正常组织（χ2 = 13.630，P = 0.0000）和良性肿瘤（χ2 = 11.797，P = 0.000）。SKOV-3和CAOV3中存在甲基化，而3AO中未检测到。基因表达与启动子甲基化之间存在相关性（r = 11.589，P = 0.002），尤其是在Hap I1位点（r = 11.640，P = 0.004）。SKOV-3和CAOV3细胞系中也检测到甲基化，但3AO细胞系中未检测到。
卵巢上皮癌细胞中存在OPCML基因缺失。基因启动子甲基化，尤其是Hap II基序，可能是导致OPCML表达受抑制的途径之一。
