Methylation Status Of Promoter Of Mismatch Repair Gene PpENK In Glioma

Object：DNA methylation is an epigenetic event that affects genomic stability and contributessignificantly to the development of cancer. Aberrant methylation of DNA is frequentlyfound in tumor cells and tumor suppressor genes hyper methylation may also play animportant role in glioma. This study adopts nest PCR (nPCR) and hydrogen sulfite saltafter modification sequencing method (BSP method) detecting candidatedtumor-suppressor genes promoter methylation in surgical resection of gliomas and areathis group of patients postoperative patients receied follow-up survival, discussing theppENK gene promoter methylation gliomas occurrence and development, therelationship between role and clinical disease material.Methods：Methylation status of the ppENK promoter region was assayed in32glioma tissues and10normal brain tissues by nested polymerase chain reaction (nPCR) and Bisulfitesequence polymerase chain reaction (BSP). Statistical methods were adapted to discussthe relationship between the ppENK gene promoter methylation gliomas occurrence andclinical disease material (pathological grades, patient’s age, gender and tumor sizefactors). The32patients with glioma patients were not line, preoperative chemotherapyand radiation, collect resection of the tumor tissue confirmed by pathology. Meanwhilecollecting10cases of normal brain tissue were compared.The results：No methylation of ppENK promoter was detected in the10normal brain tissues.BSP showed that the ppENK promoter region was hypermethylated in13of the32 glioma tissues and no methylation of ppENK promoter was detected in the10normalbrain tissues. The promoter hypermethylation ratio of ppENK gene in glioma tissues(40.6%) was significantly higher than that in normal brain tissues (0%, P=0.015).Moreover, we also found that the aberrant promoter methylation of ppENK gene wassignificantly correlated with tumor stage (P=0.006), but not correlated with age, sex andtumor types of patients (P=0.154,0.961and0.694, respectively). The rate (21.1%) ofppENK promoter methylation in grades Ⅰ~Ⅱ gliomas was significantly lower than that(69.2%) in grades Ⅲ~Ⅳ gliomas (P<0.05).conclusion：ppENK promoter (CpG island) hypermethylation exists in glioma, which may correlateswith the occurrence of glioma. The expression and promoter region methylation ofppENK gene in the gliomas are related to pathological grades, were not related to thepatient’s age, gender and tumor size factors. ppENK as the candidated tumor-suppressorgene promoter methylation plays an important role in clinical diagnosis and treatment ofglioma.