中国癌症杂志
中國癌癥雜誌
중국암증잡지
CHINA ONCOLOGY
2014年
8期
568-574
,共7页
崔建利%郭炜%郭艳丽%沈素朋%董稚明
崔建利%郭煒%郭豔麗%瀋素朋%董稚明
최건리%곽위%곽염려%침소붕%동치명
贲门腺癌%甲基化%RASSF10基因
賁門腺癌%甲基化%RASSF10基因
분문선암%갑기화%RASSF10기인
Gastric cardia adenocarcinoma%Methylation%RASSF10 gene
背景与目的:Ras相关域家族10基因(Ras-association domain family 10,RASSF10)在多种肿瘤组织中具有肿瘤抑制功能,然而在贲门腺癌组织中的研究尚未见报道。检测贲门腺癌(gastric cardia adenocarcinoma,GCA)组织中RASSF10基因的甲基化状态及表达情况,进一步探讨RASSF10基因在GCA发生、发展中的作用。方法:分别应用甲基化特异性聚合酶链式反应(methylation specific polymerase chain reaction,MSP)、逆转录-聚合酶链式反应(reverse transcription-polymerase chain reaction,RT-PCR)及免疫组织化学方法检测81例GCA患者癌组织及癌旁正常组织中RASSF10基因的甲基化状态及mRNA和蛋白表达情况。结果:RASSF10基因在GCA组织中的启动子区甲基化率(64.2%,52/81)显著高于癌旁正常组织(21.0%,17/81,P<0.05),并与肿瘤组织的TNM分期、分化程度及淋巴结转移相关(P均<0.05)。RASSF10基因在GCA组织中的mRNA表达量(0.57±0.05)显著低于癌旁正常组织(0.78±0.02,P<0.05),并与肿瘤组织的TNM分期及淋巴结转移相关(P均<0.05)。RASSF10蛋白在GCA组织中的阳性表达率(31.1%,26/81)明显低于癌旁正常组织(71.6%,58/81,P<0.05),并与肿瘤组织的TNM分期、分化程度及淋巴结转移相关(P均<0.05)。RASSF10基因在GCA组织中的甲基化率与其蛋白表达呈明显的负相关。结论:RASSF10基因启动子区的异常高甲基化导致的基因沉默可能是GCA发生的机制之一。
揹景與目的:Ras相關域傢族10基因(Ras-association domain family 10,RASSF10)在多種腫瘤組織中具有腫瘤抑製功能,然而在賁門腺癌組織中的研究尚未見報道。檢測賁門腺癌(gastric cardia adenocarcinoma,GCA)組織中RASSF10基因的甲基化狀態及錶達情況,進一步探討RASSF10基因在GCA髮生、髮展中的作用。方法:分彆應用甲基化特異性聚閤酶鏈式反應(methylation specific polymerase chain reaction,MSP)、逆轉錄-聚閤酶鏈式反應(reverse transcription-polymerase chain reaction,RT-PCR)及免疫組織化學方法檢測81例GCA患者癌組織及癌徬正常組織中RASSF10基因的甲基化狀態及mRNA和蛋白錶達情況。結果:RASSF10基因在GCA組織中的啟動子區甲基化率(64.2%,52/81)顯著高于癌徬正常組織(21.0%,17/81,P<0.05),併與腫瘤組織的TNM分期、分化程度及淋巴結轉移相關(P均<0.05)。RASSF10基因在GCA組織中的mRNA錶達量(0.57±0.05)顯著低于癌徬正常組織(0.78±0.02,P<0.05),併與腫瘤組織的TNM分期及淋巴結轉移相關(P均<0.05)。RASSF10蛋白在GCA組織中的暘性錶達率(31.1%,26/81)明顯低于癌徬正常組織(71.6%,58/81,P<0.05),併與腫瘤組織的TNM分期、分化程度及淋巴結轉移相關(P均<0.05)。RASSF10基因在GCA組織中的甲基化率與其蛋白錶達呈明顯的負相關。結論:RASSF10基因啟動子區的異常高甲基化導緻的基因沉默可能是GCA髮生的機製之一。
배경여목적:Ras상관역가족10기인(Ras-association domain family 10,RASSF10)재다충종류조직중구유종류억제공능,연이재분문선암조직중적연구상미견보도。검측분문선암(gastric cardia adenocarcinoma,GCA)조직중RASSF10기인적갑기화상태급표체정황,진일보탐토RASSF10기인재GCA발생、발전중적작용。방법:분별응용갑기화특이성취합매련식반응(methylation specific polymerase chain reaction,MSP)、역전록-취합매련식반응(reverse transcription-polymerase chain reaction,RT-PCR)급면역조직화학방법검측81례GCA환자암조직급암방정상조직중RASSF10기인적갑기화상태급mRNA화단백표체정황。결과:RASSF10기인재GCA조직중적계동자구갑기화솔(64.2%,52/81)현저고우암방정상조직(21.0%,17/81,P<0.05),병여종류조직적TNM분기、분화정도급림파결전이상관(P균<0.05)。RASSF10기인재GCA조직중적mRNA표체량(0.57±0.05)현저저우암방정상조직(0.78±0.02,P<0.05),병여종류조직적TNM분기급림파결전이상관(P균<0.05)。RASSF10단백재GCA조직중적양성표체솔(31.1%,26/81)명현저우암방정상조직(71.6%,58/81,P<0.05),병여종류조직적TNM분기、분화정도급림파결전이상관(P균<0.05)。RASSF10기인재GCA조직중적갑기화솔여기단백표체정명현적부상관。결론:RASSF10기인계동자구적이상고갑기화도치적기인침묵가능시GCA발생적궤제지일。
Background and purpose:RASSF10 acts as a kind of tumor suppressor in various tumor tissues, but researches in cardiac adenocarcinoma has not been reported. This study aimed to detect the methylation status and expression ofRas-association domain family 10 (RASSF10) in gastric cardia adenocarcinoma (GCA), and explore its role in occurrence and development of GCA.Methods:Methylation speciifc polymerase chain reaction (MSP), reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry method were respectively used to detect methylation status, mRNA expression and protein expression ofRASSF10 in 81 GCA tissues and corresponding normal tissues.Results:The promoter methylation frequency ofRASSF10 in GCA tissues (64.20%, 52/81) was signiifcantly higher than that in corresponding normal tissues (20.99%, 17/81,P<0.05), and was closely correlated with TNM stages, differential degree and lymph node metastasis (P<0.05). RASSF10 mRNA expression in GCA tissues (0.57±0.05) was significantly lower than that in corresponding normal tissues (0.78±0.02,P<0.05), and was closely correlated with TNM stages and lymph node metastasis (P<0.05). Protein expression of RASSF10 in GCA tissues (31.10%, 26/81) was signiifcantly lower than that in corresponding normal tissues (71.60%, 58/81,P<0.05), and was closely correlated with TNM stages, differential degree and lymph node metastasis (P<0.05). The promoter methylation frequency ofRASSF10 in GCA tissues was inversely related to its protein expression.Conclusion:Inactivation of RASSF10 caused by aberrantmethylation in the promoter region may be closely correlated with the GCA tumorgenesis.