中国临床神经科学
中國臨床神經科學
중국림상신경과학
CHINESE JOURNAL OF CLINICAL NEUROSCIENCES
2015年
4期
406-410
,共5页
蔡晓平%高丽%何跃%董艳娟%贾建军
蔡曉平%高麗%何躍%董豔娟%賈建軍
채효평%고려%하약%동염연%가건군
神经胶质瘤%miRNA-449基因%定量PCR检测
神經膠質瘤%miRNA-449基因%定量PCR檢測
신경효질류%miRNA-449기인%정량PCR검측
glioblastoma%miRNA-449 gene%quantitative real-time PCR
目的:研究miRNA-449基因表达水平与神经胶质瘤的发生的相关性分析。方法选择神经胶质瘤患者66例(胶质瘤组),胶质瘤组再按分级分为2个亚组:低级别胶质瘤组(30例);高级别胶质瘤组(36例)。另选择颅内减压术脑外伤患者的正常脑组织标本10例为对照组。提取脑组织,经实时定量PCR扩增进行荧光定量分析miRNA-449基因表达,采用MS-PCR方法检测miRNA-449甲基化水平。结果定量PCR检测结果显示:对照组患者脑组织miRNA-449基因表达水平高于胶质瘤组(P=0.000);高级别胶质瘤组miRNA-449基因表达水平低于低级别胶质瘤组(P=0.044)。对66例脑胶质瘤患者miRNA-449基因启动子区甲基化水平进行检测,并与其表达水平进行相关性分析,发现在高甲基化患者miRNA-449基因表达水平低于无甲基化患者(P=0.0002)。结论 miRNA-449基因表达降低可能与miRNA-449基因启动子区甲基化水平有一定相关性,且可能参与神经胶质瘤的发生发展,为疾病进展的早期监测提供分子理论依据。
目的:研究miRNA-449基因錶達水平與神經膠質瘤的髮生的相關性分析。方法選擇神經膠質瘤患者66例(膠質瘤組),膠質瘤組再按分級分為2箇亞組:低級彆膠質瘤組(30例);高級彆膠質瘤組(36例)。另選擇顱內減壓術腦外傷患者的正常腦組織標本10例為對照組。提取腦組織,經實時定量PCR擴增進行熒光定量分析miRNA-449基因錶達,採用MS-PCR方法檢測miRNA-449甲基化水平。結果定量PCR檢測結果顯示:對照組患者腦組織miRNA-449基因錶達水平高于膠質瘤組(P=0.000);高級彆膠質瘤組miRNA-449基因錶達水平低于低級彆膠質瘤組(P=0.044)。對66例腦膠質瘤患者miRNA-449基因啟動子區甲基化水平進行檢測,併與其錶達水平進行相關性分析,髮現在高甲基化患者miRNA-449基因錶達水平低于無甲基化患者(P=0.0002)。結論 miRNA-449基因錶達降低可能與miRNA-449基因啟動子區甲基化水平有一定相關性,且可能參與神經膠質瘤的髮生髮展,為疾病進展的早期鑑測提供分子理論依據。
목적:연구miRNA-449기인표체수평여신경효질류적발생적상관성분석。방법선택신경효질류환자66례(효질류조),효질류조재안분급분위2개아조:저급별효질류조(30례);고급별효질류조(36례)。령선택로내감압술뇌외상환자적정상뇌조직표본10례위대조조。제취뇌조직,경실시정량PCR확증진행형광정량분석miRNA-449기인표체,채용MS-PCR방법검측miRNA-449갑기화수평。결과정량PCR검측결과현시:대조조환자뇌조직miRNA-449기인표체수평고우효질류조(P=0.000);고급별효질류조miRNA-449기인표체수평저우저급별효질류조(P=0.044)。대66례뇌효질류환자miRNA-449기인계동자구갑기화수평진행검측,병여기표체수평진행상관성분석,발현재고갑기화환자miRNA-449기인표체수평저우무갑기화환자(P=0.0002)。결론 miRNA-449기인표체강저가능여miRNA-449기인계동자구갑기화수평유일정상관성,차가능삼여신경효질류적발생발전,위질병진전적조기감측제공분자이론의거。
Aim To evaluate the signiifcance of miRNA-449 expression in glioblastoma. Methods Sixty six patients with glioblastoma and 10 healthy donors were adopted in this study. RNA was isolated from cerebra tissue, and quantitative real-time PCR (Q-PCR) were used to detect the levels of miRNA-449 gene in health donors and newly diagnosed glioblastoma patients. Results Q-PCR analysis showed that the levels of miRNA-449 in glioblastoma group were lower than those in healthy donors group (P=0.000). Furthermore, the miRNA-449 expression was lower in high stage disease than that in low stage group (P=0.044). The methylation levels of the miRNA-449 was detected by MS-PCR. The levels of miRNA-449 in high methylation group were found to be lower than that in low methylation group (P=0.000 2). Conclusion The aberrant expression of the miRNA-449 gene was perhaps correlated with the levels of miRNA-449 methylation and may be involved in the occurrence and progression of glioblastoma, which provided the molecular basis of the early monitoring disease progression.