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作 者:胡成平[1] 宾亮华[2] 湛凤凰[1] 曹立明 李桂源[2]
机构地区:[1]湖南医科大学附属湘雅医院呼吸科,湖南410078 [2]湖南医科大学肿瘤研究所
出 处:《肿瘤》2000年第1期21-24,共4页Tumor
摘 要:目的 探讨肺癌细胞转化生长因子β(TGFβ)信息传递通路中配体、受体及受体相互作用蛋白-1(TRIP-1)的表达功能状态。方法 分别采用免疫组化技术和Northern 杂交方法,检测65 例肺癌患者癌组织和癌旁组织中TGFβ1 、β2 及相应受体(TβRⅠ、Ⅱ)蛋白水平表达状态,以及32 例肺癌患者癌组织和配对正常肺组织中TRIP-1m RNA 表达变化。结果 TGFβ1 在肺癌组织中的表达阳性率(42.3% )和表达强度(0.41±0.04)明显低于TGFβ2(73.1% ,2.03±0.11)和相应的癌旁组织(66.0% ,1.26±0.11),且TGFβ1β2 的表达状态与肺癌细胞的分化程度有关,低分化癌明显低于中-高分化癌(分别为P< 0.05,P<0.005)。与正常肺组织相比,癌组织中TβRⅠ、Ⅱ表达虽无明显降低,但其中TβRⅡ表达强度明显弱于TβRⅠ,同时,TRIP-1 m RNA表达明显降低(0.66±0.15 vs 1.88±0.31,P< 0.01)。结论 肺癌细胞TGFβ信息传递通路中配体,受体及受体相互作用蛋白的表达功能存在不同程度的缺陷。Objective To explore the functional status of ligants,receptors and TGF receptor interacting protein 1(TRIP 1) in transforming growth factor beta (TGF β) signal transduction pathway in lung cancer cells.Methods An immunohistochemical study was undertaken to analyze TGF β 1、β 2 and TGF β types Ⅰ and Ⅱ receptor protein on the cancerous and paracancerous tissue specimens from 53 pateints with primary lung cancer.Expression of TRIP 1 mRNA was detected in the cancerous and normal lung tissues of 12 patients using Northern blot hybridization.Results The expression of TGF β 1 protein was much lower than TGF β 2 in the cancerous tissue and lower than that in paracancerous tissue( P <0 05).Meanwhile,the expression status of TGF β protein was related to degree of lung cancer cell differentiation,the protein level in poorly differentiated cancer was significantly lower than that in well and moderately differentiated cancer( P <0 05). There was no significant difference in the expressive level of TGF β type Ⅰ and Ⅱreceptor proteins between cancerous and paracancerous tissues,but the expression of TRIP 1 mRNA,which is a signaling pathway associated facotr,was much lower in cancerous tissue than that in normal lung tissue ( P <0 01).Conclusion There are different degree of defects in the expressive function of the ligants、receptors and TRIP 1 or TGF β signal transduction pathway in lung cancer cells:the lower expression of TRIP 1 might be another mechanism of inactivation of TGF beta signaling pathway.$$$$
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