中华胃肠外科杂志
中華胃腸外科雜誌
중화위장외과잡지
CHINESE JOURNAL OF GASTROINTESTINAL SURGERY
2011年
7期
538-541
,共4页
李臣%董坚%陈明清%李文亮%任俊宇%陈圣雄%李秋恬%耿计伟%缪延栋%杨静
李臣%董堅%陳明清%李文亮%任俊宇%陳聖雄%李鞦恬%耿計偉%繆延棟%楊靜
리신%동견%진명청%리문량%임준우%진골웅%리추념%경계위%무연동%양정
上皮钙黏素%β-连接素%结肠肿瘤%甲基化
上皮鈣黏素%β-連接素%結腸腫瘤%甲基化
상피개점소%β-련접소%결장종류%갑기화
E-cadherin%β-catenin%Colonic neoplasms%Methylation
目的 探讨上皮钙黏素基因(CDH1)启动子甲基化与结肠癌上皮钙黏素(E-cadherin)及β-连接素(β-catenin)的表达及临床病理特征的关系.方法 采用甲基化特异性PCR技术检测68例结肠腺癌组织、癌旁组织及正常黏膜组织中CDH1基因启动子甲基化的状况.采用免疫组织化学法检测E-cadherin及β-catenin蛋白的表达.结果 癌旁组织及癌组织中CDH1启动子甲基化的阳性表达分别为32.4%(22/68)、57.4%(39/68),正常组织均为阴性表达(P<0.05).E-cadherin在正常组织、癌旁组织及腺癌组织中阳性表达率分别为92.6%、66.2%和44.1%.正常组织中β-catenin均表达于细胞膜上,无胞质和(或)胞核表达,而β-catenin在癌旁组织及癌组织中胞质和(或)胞核表达分别为29.4%和50.0%.CDH1基因启动子甲基化阳性率与E-cadherin表达则呈负相关(r=-0.312,P=0.01),与β-catenin胞质和(或)胞核表达呈正相关(r=0.309,P=0.018).CDH1基因启动子甲基化及E-cadherin、β-catenin的异常表达均与结肠癌分化程度及转移密切相关(P<0.05).结论 CDH1基因启动子甲基化可能是导致结肠癌E-cadherin与β-catenin异常表达及肿瘤侵袭性增强的重要原因.
目的 探討上皮鈣黏素基因(CDH1)啟動子甲基化與結腸癌上皮鈣黏素(E-cadherin)及β-連接素(β-catenin)的錶達及臨床病理特徵的關繫.方法 採用甲基化特異性PCR技術檢測68例結腸腺癌組織、癌徬組織及正常黏膜組織中CDH1基因啟動子甲基化的狀況.採用免疫組織化學法檢測E-cadherin及β-catenin蛋白的錶達.結果 癌徬組織及癌組織中CDH1啟動子甲基化的暘性錶達分彆為32.4%(22/68)、57.4%(39/68),正常組織均為陰性錶達(P<0.05).E-cadherin在正常組織、癌徬組織及腺癌組織中暘性錶達率分彆為92.6%、66.2%和44.1%.正常組織中β-catenin均錶達于細胞膜上,無胞質和(或)胞覈錶達,而β-catenin在癌徬組織及癌組織中胞質和(或)胞覈錶達分彆為29.4%和50.0%.CDH1基因啟動子甲基化暘性率與E-cadherin錶達則呈負相關(r=-0.312,P=0.01),與β-catenin胞質和(或)胞覈錶達呈正相關(r=0.309,P=0.018).CDH1基因啟動子甲基化及E-cadherin、β-catenin的異常錶達均與結腸癌分化程度及轉移密切相關(P<0.05).結論 CDH1基因啟動子甲基化可能是導緻結腸癌E-cadherin與β-catenin異常錶達及腫瘤侵襲性增彊的重要原因.
목적 탐토상피개점소기인(CDH1)계동자갑기화여결장암상피개점소(E-cadherin)급β-련접소(β-catenin)적표체급림상병리특정적관계.방법 채용갑기화특이성PCR기술검측68례결장선암조직、암방조직급정상점막조직중CDH1기인계동자갑기화적상황.채용면역조직화학법검측E-cadherin급β-catenin단백적표체.결과 암방조직급암조직중CDH1계동자갑기화적양성표체분별위32.4%(22/68)、57.4%(39/68),정상조직균위음성표체(P<0.05).E-cadherin재정상조직、암방조직급선암조직중양성표체솔분별위92.6%、66.2%화44.1%.정상조직중β-catenin균표체우세포막상,무포질화(혹)포핵표체,이β-catenin재암방조직급암조직중포질화(혹)포핵표체분별위29.4%화50.0%.CDH1기인계동자갑기화양성솔여E-cadherin표체칙정부상관(r=-0.312,P=0.01),여β-catenin포질화(혹)포핵표체정정상관(r=0.309,P=0.018).CDH1기인계동자갑기화급E-cadherin、β-catenin적이상표체균여결장암분화정도급전이밀절상관(P<0.05).결론 CDH1기인계동자갑기화가능시도치결장암E-cadherin여β-catenin이상표체급종류침습성증강적중요원인.
Objective To investigate the relationship between methylation of the CDH1 gene promoter on the expression of E-cadherin and β-catenin, and to evaluate the correlation with clinicopathological characteristics of the colonic carcinoma. Methods Methylation specific PCR (MSP) was used to detect CDH1 gene promoter methylation in the cancer tissue, adjacent tissues and normal tissues in 68 patients. The expression of E-cadherin and β-catenin was determined by immunohistochemistry staining. Results The positive rate of CDH1 gene promoter methylation was 32.4% in adjacent tissues and 57.4% in cancer tissue, while no detectable methylation was found in all the normal tissues. The difference was statistically significant. The positive rate of E-cadherin was 92.6% in the normal tissues, 66.2% in the adjacent tissues and 44.1% in the cancer tissues. In all normal tissues, β-catenin was expressed only at the cellular membrane but not in the cytosol or nucleus, while the expression of β-catenin was present in the cytosol or nucleus in 29.4% of the adjacent tissues and 50.0% of the cancer tissues. The positive rate of CDH1 gene promoter methylation was negatively correlated with E-cadherin expression (r =-0.312,P =0.01) and positively correlated with β-catenin cytosolic/nucleus expression(r=0.309,P=0.018). The differentiation and metastasis of colonic carcinoma were associated with the aberrant expression of E-cadherin, β-catenin, and methylation of CDH1 promoter (P<0.05). Conclusion CDH1 gene promoter methylation may lead to aberrant expression of E-cadherin and β-catenin in colonic carcinoma, and may play an important role in promoting the invasion of tumor.