CAJ | 학술논문

目的：探讨p57 kip2、Cyclin D1在人子宫内膜癌发生、发展中的作用。方法选取子宫内膜样腺癌( endometrioid adenocar-cinoma, EA)100例、子宫内膜上皮内瘤变(endometrial intraepithelial neoplasia, EIN)20例、子宫内膜增生性病变20例、增生期子宫内膜组织20例；选取不同子宫内膜细胞[高分化子宫内膜癌细胞( Ishikawa)、中分化子宫内膜癌细胞( JEC)、低分化子宫内膜癌细胞(KLE)及正常子宫内膜细胞(ESC)]进行细胞培养。应用免疫组化EliVision法检测不同子宫内膜组织中p57kip2、Cyclin D1蛋白的表达；Western blot法检测不同子宫内膜细胞中p57 kip2、Cyclin D1蛋白的表达。结果 p57 kip2蛋白在EIN组织中表达最高,在增生期子宫内膜、EA、子宫内膜增生性病变组织中表达逐渐降低,子宫内膜增生性病变与EIN组织中p57 kip2蛋白表达差异有统计学意义(P<0.05)。 Cyclin D1蛋白在EA组织中表达最高,在增生期子宫内膜组织中表达最低,在子宫内膜增生性病变组织、EIN组织中表达依次增高,差异均有显著性( P<0.01)。 p57 kip2、Cyclin D1蛋白在EA组织中的表达随着组织学分级的增高呈依次递减趋势,但仅p57 kip2蛋白表达和组织学分级有关( P<0.05)。 p57 kip2蛋白在KLE中表达最高,在ESC中表达最低,两组相比差异有显著性( P<0.05)；Cyclin D1在JEC、Ishikawa中的表达高于ESC,差异均有显著性( P<0.05)。结论 p57kip2、Cyclin D1均参与子宫内膜癌的发生、发展。 Cyclin D1表达是子宫内膜癌发生的早期事件,可能还存在异常合成的p57 kip2蛋白,其协同Cyclin D1促进子宫内膜的恶性转化。联合检测p57 kip2、Cyclin D1在子宫内膜癌中的表达,对预测子宫内膜癌患者预后有一定的临床意义。
목적：탐토p57 kip2、Cyclin D1재인자궁내막암발생、발전중적작용。방법선취자궁내막양선암( endometrioid adenocar-cinoma, EA)100례、자궁내막상피내류변(endometrial intraepithelial neoplasia, EIN)20례、자궁내막증생성병변20례、증생기자궁내막조직20례；선취불동자궁내막세포[고분화자궁내막암세포( Ishikawa)、중분화자궁내막암세포( JEC)、저분화자궁내막암세포(KLE)급정상자궁내막세포(ESC)]진행세포배양。응용면역조화EliVision법검측불동자궁내막조직중p57kip2、Cyclin D1단백적표체；Western blot법검측불동자궁내막세포중p57 kip2、Cyclin D1단백적표체。결과 p57 kip2단백재EIN조직중표체최고,재증생기자궁내막、EA、자궁내막증생성병변조직중표체축점강저,자궁내막증생성병변여EIN조직중p57 kip2단백표체차이유통계학의의(P<0.05)。 Cyclin D1단백재EA조직중표체최고,재증생기자궁내막조직중표체최저,재자궁내막증생성병변조직、EIN조직중표체의차증고,차이균유현저성( P<0.01)。 p57 kip2、Cyclin D1단백재EA조직중적표체수착조직학분급적증고정의차체감추세,단부p57 kip2단백표체화조직학분급유관( P<0.05)。 p57 kip2단백재KLE중표체최고,재ESC중표체최저,량조상비차이유현저성( P<0.05)；Cyclin D1재JEC、Ishikawa중적표체고우ESC,차이균유현저성( P<0.05)。결론 p57kip2、Cyclin D1균삼여자궁내막암적발생、발전。 Cyclin D1표체시자궁내막암발생적조기사건,가능환존재이상합성적p57 kip2단백,기협동Cyclin D1촉진자궁내막적악성전화。연합검측p57 kip2、Cyclin D1재자궁내막암중적표체,대예측자궁내막암환자예후유일정적림상의의。
Purpose To study the effects of p57kip2, Cyclin D1 on the carcinogenesis and progression of endometrial carcinoma. Meth-ods 100 cases of endometrial adenocarcinoma ( EA) , 20 cases of endometrial intraepithelial neoplasia ( EIN) , 20 cases of hyperpla-sia lesion, 20 cases of endometrial proliferative phase were selected. Different endometrial cells ( well-differentiated endometrial cancer cells Ishikawa, moderately differentiated endometrial cancer cells JEC, poorly differentiated endometrial cancer cells KLE and normal endometrial cells ESC) were cultured. Protein expression of p57kip2, Cyclin D1 was measured by immunohistochemical EliVision meth-ods. The expression of p57kip2, Cyclin D1 protein in different endometrial cells was detected by Western blot. Results The highest expression of p57kip2 protein was in EIN, the higher expression was in endometrial proliferative phase, the low expression was in EA and the lowest expression was in hyperplasia lesions, but only the expression of p57kip2 protein in EIN was higher than that in hyperplasia le-sions (P<0.05). The highest expression of Cyclin D1 protein was in EA and the lowest expression of Cyclin D1 protein was in endom-etrial proliferative phase, expression of Cyclin D1 protein increased gradually in hyperplasia lesions and EIN, p57kip2, Cyclin D1 pro-tein expression in the tissue of EA increased along with the histological grade, all present decreasing trend, but only p57kip2 protein ex-pression related to histological grade ( P<0.05 ) . The highest expression of p57 kip2 protein was in KLE and the lowest expression of p57kip2 protein was in ESC, but only the expression of p57kip2 protein in KLE was higher than that in ESC (P<0.05). The expression of Cyclin D1 in JEC, Ishikawa higher than that in ESC (P<0.05). Conclusion p57kip2, Cyclin D1 are involved in the occurrence and development of endometrial carcinoma, Cyclin D1 is an early event in endometrial carcinoma, but there may also be have abnormal p57kip2 protein by synthesized, synergistically. Cyclin D1 promoting endometrial malignant transformation. Combined detection of p57kip2, Cyclin D1 expression in endometrial carcinoma, to predict the prognosis of endometrial carcinoma has a certain clinical signifi-cance.