OBJECTIVES: To study the relationship between promoter methylation and mRNA expressions of EMP3 and PCDH-gamma-A11 genes in human glioma, and to analyze the regulation mechanism of promoter methylation in the progression of glioma. METHODS: The promoter methylation of EMP3 and PCDH-gamma-A11 was studied by a methylation specific PCR in 88 primary astrocytoma, 10 normal brain tissues and 2 glioma cell lines. The mRNA expressions were detected by real-time PCR in 30 primary glioma and 10 normal brain tissues. The correlations of their promoter methylation, mRNA expressions and clinicopathologic characteristics were analyzed. The promoter methylation were also detected in U251 and SHG-44 cell lines. RESULTS: The promoter methylation of EMP3 was detected in 42 tumors (47.7%) and the methylation of PCDH-gamma-A11 was detected in 76 tumors (86.4%). Their mRNA expressions were all significantly decreased in different pathological grade astrocytomas compared to the normal brain tissues (P < 0.01). Their expressions were suppressed but could be reactivated by 5-aza-deoxycytidine in U251 and SHG-44 cell lines. CONCLUSIONS: The promoter methylation of EMP3 and PCDH-gamma-A11 genes may lead to the down-regulation of their mRNA levels in glioma. The promoter methylation and mRNA expressions of EMP3 and PCDH-gamma-A11 are closely related with the malignant development of glioma. The promoter methylation of the two genes may provide clues to evaluation of glioma malignancy as well as its prognosis. It also gives us an insight for future glioma medical therapy with a demethylating agent.
OBJECTIVES: To study the relationship between promoter methylation and mRNA expressions of EMP3 and PCDH-gamma-A11 genes in humanglioma, and to analyze the regulation mechanism of promoter methylation in the progression of glioma. METHODS: The promoter methylation of EMP3 and PCDH-gamma-A11 was studied by a methylation specific PCR in 88 primary astrocytoma, 10 normal brain tissues and 2 glioma cell lines. The mRNA expressions were detected by real-time PCR in 30 primary glioma and 10 normal brain tissues. The correlations of their promoter methylation, mRNA expressions and clinicopathologic characteristics were analyzed. The promoter methylation were also detected in U251 and SHG-44 cell lines. RESULTS: The promoter methylation of EMP3 was detected in 42 tumors (47.7%) and the methylation of PCDH-gamma-A11 was detected in 76 tumors (86.4%). Their mRNA expressions were all significantly decreased in different pathological grade astrocytomas compared to the normal brain tissues (P < 0.01). Their expressions were suppressed but could be reactivated by 5-aza-deoxycytidine in U251 and SHG-44 cell lines. CONCLUSIONS: The promoter methylation of EMP3 and PCDH-gamma-A11 genes may lead to the down-regulation of their mRNA levels in glioma. The promoter methylation and mRNA expressions of EMP3 and PCDH-gamma-A11 are closely related with the malignant development of glioma. The promoter methylation of the two genes may provide clues to evaluation of glioma malignancy as well as its prognosis. It also gives us an insight for future glioma medical therapy with a demethylating agent.
Authors: Xiao Chun Hong; Yuan Jian Fen; Guo Chun Yan; Hong Hong; Cao Hong Yan; Li Wei Bing; Yu Hai Zhong Journal: Mol Med Rep Date: 2015-09-14 Impact factor: 2.952