E-Cadherin基因在乳腺癌中的表达及临床意义

目的：研究E－Cadherin基因在乳腺癌中的表达及临床意义。方法：应用免疫组织化学方法（SABC法），检测92例乳腺癌组织E－Cadherin基因蛋白的表达，同时观察与腋淋巴结和远处转移的关系。结果：乳腺癌E－Cadherin基因表达阳性率为48．9％（45／92）。无淋巴结转移组E－Cadherin阳性率62．2％（28／47），明显高于淋巴结受累组表达阳性率36．2％（17／47）（P＜0．05）。E－Cadherin阳性组远处转移率15．6％（7／45），低于阴性组远处转移率34％（16／47，P＜0．05），E－Cadherin基因表达与疾病缓解期无关。结论：提示E－Cadherin基因在乳腺癌病程中起重要作用，对筛选乳腺癌术后高危转移患者，加强随访诊治有一定参考意义。E－Cadherin低表达可能提示病人预后不良。     

前列腺癌组织P504S、E-Cadherin和bcl-2蛋白表达及意义

目的分析前列腺癌中P504S、E-Cadherin和bcl-2蛋白的表达情况,探讨其在前列腺癌诊断及预后判断中的意义。方法应用免疫组织化学(Max Vision)法检测45例前列腺腺泡腺癌、6例前列腺高级别上皮内肿瘤及10例前列腺增生组织中P504S、E-Cadherin和bcl-2蛋白的表达情况。结果 P504S蛋白阳性率前列腺癌组(84.4%)明显高于前列腺高级别上皮内肿瘤组(50.0%)和前列腺增生组(0%)(P<0.05);E-Cadherin蛋白阳性率前列腺癌组(42.2%)和前列腺高级别上皮内肿瘤组(33.3%)明显低于前列腺增生组(100%)(P<0.05);bcl-2蛋白阳性率前列腺癌组(60.0%)明显高于前列腺高级别上皮内肿瘤组(16.7%)和前列腺增生组(20.0%)(P<0.05)。前列腺癌Gleason 8～10分组E-Cadherin蛋白的表达率(31.8%)明显低于2～4分组(83.3%)(P<0.05);8～10分组bcl-2蛋白的表达率(68.2%)明显高于2～4分组(33.3%)(P<0.05)。前列腺癌Gleason8～10分组(18.2%)和5～7分组(17.6%)E-Cadherin蛋白的强阳性表达率明显低于2～4分组(83.3%)(P<0.05)。前列腺癌组P504S蛋白阳性同时E-Cadherin蛋白阴性的比率(51.1%)明显高于前列腺增生组(0%)(P<0.05);前列腺癌组P504S蛋白阳性同时bcl-2阳性的比率(57.8%)明显高于前列腺增生组(0%)(P<0.05)。结论 P504S高表达、bcl-2高表达有助于前列腺癌的诊断;联合检测P504S和E–Cadherin,P504S和bcl-2的表达,可以提高诊断前列腺癌的准确性。     

大肠癌组织蛋白酶D和E-Cadherin的表达及意义

目的 检测组织蛋白酶D(Cathepsin D.简称Cath-D)、E-Cadherin在大肠癌中的表达及其临床意义,探讨其在大肠癌中的作用及两标记物间的相关性.方法 应用免疫组化方法研究32例大肠癌手术标本和相应癌旁的正常组织标本及12例大肠腺瘤组织中Cath-D,E-Cadherin的表达情况.结果 ①Cath-D在大肠癌和正常组织及腺瘤组织中的阳性表达率分别为71.9%,8.3%,0;E-Cadherin分别为34.4%,75%,和83.3%,两者在肠癌组织与腺瘤、正常组织表达率均有显著差异(P＜0.01).②两者均与大肠癌的浸润深度、淋巴结转移、肝转移及Duke's分期有密切关系,E-Cadherin与肿瘤分化程度亦相关.③Cath-D与E-Cadherin无显著相关性.结论 Cath-D与E-Cadherin在大肠癌的发生发展及转移中起重要作用,可作为预测预后的指标.     

E-Cadherin在Ⅰ型子宫内膜癌中的表达

目的:探讨上皮钙黏附蛋白-E在Ⅰ型子宫内膜癌中的表达及意义.方法:采用免疫组织化学EnVision法检测30例增生期子宫内膜、36例单纯性增生宫内膜、50例不典型增生内膜及55例Ⅰ型子宫内膜癌组织中E-Cadherin蛋白的表达.结果:从增生期子宫内膜、单纯性增生宫内膜、不典型增生宫内膜到Ⅰ型子宫内膜癌,正常的E-cadherin表达逐渐降低,异质表达E-cadherin逐渐升高(P＜0.01).内膜癌中E-cadherin蛋白表达与年龄及组织学分级无关(P＞0.05).结论:E-cadherin蛋白的表达与Ⅰ型子宫内膜癌的发生发展有关.     

CD44v6、E-Cadherin在乳腺癌中的表达及意义

目的:研究乳腺癌组织中CD44v6和E-Cadherin的表达,探讨其表达与乳腺癌各临床病理特征之间的关系,分析CD44v6及E-Cadherin表达之间的相关性。方法:应用免疫组织化学染色方法(SP法)检测75例乳腺癌组织、40例癌旁乳腺组织、20例正常乳腺组织中CD44v6、E-Cadherin的表达,分析其表达与临床病理学特征的关系以及CD44v6与E-Cadher-in表达的相关性。结果:E-Cadherin表达率乳腺癌组织<正常乳腺组织(P<0.01)、癌肿>2 cm者<癌肿<2 cm者(P<0.01);Ⅲ期乳腺癌<Ⅱ期乳腺癌<Ⅰ期乳腺癌(P<0.05);有淋巴结转移者<无淋巴结转移者(P<0.05)。CD44v6表达率乳腺癌组织>正常乳腺组织(P<0.01)、癌肿>3 cm者>癌肿<3 cm者(P<0.01);Ⅲ期乳腺癌>Ⅱ期乳腺癌>Ⅰ期乳腺癌(P<0.05);有淋巴结转移者>无淋巴结转移者(P<0.05)。CD44v6与E-Cadherin之间存在负相关。结论:CD44v6及E-Cadherin表达水平与乳腺癌临床分期、淋巴结转移、组织分化程度相关,两者之间的关系密切。联合检测可能对乳腺癌的辅助诊断具有一定的临床意义。     

Expression of connexin 43 and E-cadherin in choroidal melanoma

AIM: To investigate the expression of connexin 43 and epithelial cadherin (E-cadherin) in choroidal melanoma, to explore the clinical and pathological implications of expression of these proteins, and to determine their relations with malignant features． METHODS: The expression of connexin 43 and E-cadherin in choroidal melanoma were detected by immunohist- ochemistry and correlated with clinicopathological features. RESULTS: Positive rates of connexin 43 in choroidal melanomas and benign pigmented nevus tissues were 75% and 40% respectively with significant differences between the two groups (χ2=5.607, P=0.009). Positive rates of E-cadherin in choroidal melanomas and benign pigmented nevus tissues were 40％ and 75% respectively with significant differences between the two groups (χ2=5.214, P=0.010). Significant overexpression of connexin 43 and reduction of E-cadherin expression was associated with the invasion to the sclera, and there were respectively significant differences between without and with scleral invasion groups (χ2=2.880, P=0.040; χ2=2.778, P=0.046). Overexpression of connexin 43 were correlated with tumor cell types and the expression of connexin 43 and E-cadherin may be correlated with each other. CONCLUSION: The increased expression of connexin 43 and the decreased expression of E-cadherin may be involved in the process of invasion of choroidal melanoma. The overepression of connexin 43 and reduction of E-cadherin may contribute to the development of choroidal melanoma．     

Developmental change in expression of highly polysialylated neural cell adhesion molecule in C-cells in rat thyroid gland

The expression of the neural cell adhesion molecule (NCAM), highly polysialylated NCAM, and Ecadherin was immunohistochemically studied in the calcitonin-producing cells (C-cells) of developing and adult rat thyroid glands of varying ages. In fetal and neonatal rat thyroids, almost all the C-cells displayed immunoreactivity for highly polysialylated NCAM, whereas most of the follicular cells were negative. The highly polysialylated NCAM-positive C-cells markedly decreased in number between 5 and 14 days after birth. From day 14 onward, immunoreactivity for highly polysialylated NCAM was almost negative in thyroid glands. On the other hand, the expression of immunoreactivity for NCAM peptide persisted in thyroidal C-cells throughout the life span. These results suggest that conversion of the highly polysialylated NCAM into a less sialylated form occurs in the thyroid C-cells between postnatal days 5 and 14. Intense immunoreactivity for E-cadherin was observed in the entire cell surfaces of all the C-cells and follicular cells in the rats of all ages tested. In the course of thyroid organogenesis, C-cells transiently form a cell mass, an ultimobranchial body, which is fated to disappear as the C-cells migrate diffusely into the thyroid. The duration of the polysialic acid expression in the C-cell surfaces appears to coincide with the period of C-cell migration. It is possible that the expression of highly polysialylated NCAM allows the C-cells to migrate into the thyroid by reducing the cell-to-cell adhesion of C-cells with adjacent C-cells and/or with the surrounding follicular cells.     

血小板反应蛋白-1、E—Cadherin表达与大肠癌血管生成关系

[目的]检测血小板反应蛋白-1（TSP-1）、E—Cadherin在大肠癌中的表达及与微血管密度间的关系，探讨其在大肠癌中的作用。[方法]应用免疫组化方法检测56例大肠癌手术标本和20例相应癌旁正常组织标本中TSP—1，E—Cadherin的表达情况，用CD34标记微血管并计数MVD。[结果]TSP-1和E—Cadherin在大肠癌和正常组织巾表达均有显著性差异（P〈0．01）。TSP-1和E—Cadherin均与大肠癌的分化程度、浸润深度、淋巴结转移、肝转移及Dukes分期有密切关系。TSP—1与E—Cadherin呈正相关，两者均与MVD计数呈负相关。[结论]TSP-1与E—Cadherin在大肠癌的血管生成及转移中起重要作用，且两者可能有协同作用。     

VEGF-C和E-cadherin在非小细胞肺癌中的表达及意义

目的 探讨VEGF-C和E-Cadherin在非小细胞肺癌中的表达特点及意义.方法 采用免疫组织化学SP法检测77例非小细胞肺癌组织及10例正常肺组织中VEGF-C、E-cadherin的表达,并分析两者表达与临床病理因素的关系及其之间的相关性.结果 VEGF-C、E-cadherin在77例肺癌组织中表达的阳性率分别为63.6％(49/77)和32.5％(25/77),与在10例正常肺组织中表达阳性率(分别为10％和100％)的差异有统计学意义(P＜0.05).VEGF C的过表达与肺癌的临床分期、分化程度、淋巴结转移、病理分型有关(P＜0.05),E-cadherin的低表达与肺癌的临床分期、淋巴结转移、病理分型有关(P＜0.05).VEGF-C、E-cadherin在肺癌组织的表达存在负相关(P＜0.01),相关系数rs=-0.571.结论VEGF-C高表达或E-cadherin低表达可能与肺癌的发生.     

XPC inhibits NSCLC cell proliferation and migration by enhancing E-Cadherin expression

Xeroderma pigmentosum complementation group C (XPC) protein is an important DNA damage recognition factor in nucleotide excision repair. Deletion of XPC is associated with early stages of human lung carcinogenesis, and reduced XPC mRNA levels predict poor patient outcome for non-small cell lung cancer (NSCLC). However, the mechanisms linking loss of XPC expression and poor prognosis in lung cancer are still unclear. Here, we report evidence that XPC silencing drives proliferation and migration of NSCLC cells by down-regulating E-Cadherin. XPC knockdown enhanced proliferation and migration while decreasing E-Cadherin expression in NSCLC cells with an epithelial phenotype. Restoration of E-Cadherin in these cells suppressed XPC knockdown-induced cell growth both in vitro and in vivo. Mechanistic studies showed that the loss of XPC repressed E-Cadherin expression by activating the ERK pathway and upregulating Snail expression. Our findings indicate that XPC silencing-induced reduction of E-Cadherin expression contributes, at least in part, to the poor outcome of NSCLC patients with low XPC expression.