兰州大学学报(自然科学版)
蘭州大學學報(自然科學版)
란주대학학보(자연과학판)
JOURNAL OF LANZHOU UNIVERSITY
2005年
1期
45-51
,共7页
张洪涛%赵军%陈晓峰%曾福礼
張洪濤%趙軍%陳曉峰%曾福禮
장홍도%조군%진효봉%증복례
非小细胞肺癌%转化生长因子βⅠ型受体%免疫组化%基因突变%多态性
非小細胞肺癌%轉化生長因子βⅠ型受體%免疫組化%基因突變%多態性
비소세포폐암%전화생장인자βⅠ형수체%면역조화%기인돌변%다태성
NSCLC%TGFβR Ⅰ%immunohistochemistry%gene mutation%polymorphism
转化生长因子β(TGF-β)信号转导通路的紊乱可使细胞逃避TGF-β介导的生长抑制效应,从而导致多种肿瘤的发生.本研究探讨了转化生长因子βⅠ型受体(TGFβRⅠ)在非小细胞肺癌(NSCLC)发生中的作用.采用免疫组化进行TGFβRⅠ基因的表达分析:采用单链构象多态性(SSCP)分析TGFβRⅠ基因结构的变异.结果发现37.2%NSCLC中TGFβRⅠ的表达下降,表明TGFβRⅠ在NSCLC发生中起着重要的作用.同时在TGFβRⅠ基因的第7号内含子中发现了一个单核苷酸多态性(SNP),该SNP与TGFβRⅠ的表达下降无显著关系(P>0.05).
轉化生長因子β(TGF-β)信號轉導通路的紊亂可使細胞逃避TGF-β介導的生長抑製效應,從而導緻多種腫瘤的髮生.本研究探討瞭轉化生長因子βⅠ型受體(TGFβRⅠ)在非小細胞肺癌(NSCLC)髮生中的作用.採用免疫組化進行TGFβRⅠ基因的錶達分析:採用單鏈構象多態性(SSCP)分析TGFβRⅠ基因結構的變異.結果髮現37.2%NSCLC中TGFβRⅠ的錶達下降,錶明TGFβRⅠ在NSCLC髮生中起著重要的作用.同時在TGFβRⅠ基因的第7號內含子中髮現瞭一箇單覈苷痠多態性(SNP),該SNP與TGFβRⅠ的錶達下降無顯著關繫(P>0.05).
전화생장인자β(TGF-β)신호전도통로적문란가사세포도피TGF-β개도적생장억제효응,종이도치다충종류적발생.본연구탐토료전화생장인자βⅠ형수체(TGFβRⅠ)재비소세포폐암(NSCLC)발생중적작용.채용면역조화진행TGFβRⅠ기인적표체분석:채용단련구상다태성(SSCP)분석TGFβRⅠ기인결구적변이.결과발현37.2%NSCLC중TGFβRⅠ적표체하강,표명TGFβRⅠ재NSCLC발생중기착중요적작용.동시재TGFβRⅠ기인적제7호내함자중발현료일개단핵감산다태성(SNP),해SNP여TGFβRⅠ적표체하강무현저관계(P>0.05).
Many malignant tumor cells, including non-small cell lung cancer (NSCLC) cells, are frequently resistant to transforming growth factor β (TGF-β)-mediated signal transduction. The TGF-β signal is transduced through a pair of transmembrane serine-threonine kinase receptors named receptor type Ⅰ and Ⅱ (TGFβR Ⅰ and TGFβR Ⅱ ). Reduced expression of TGFβR Ⅰ was found in various types of human carcinomas. To investigate whether the TGFβR Ⅰ gene plays a role as a tumor suppressor in the pathogenesis of NSCLC, we performed the immunohistochemical and molecule structural analyses of TGFβR Ⅰ in tumor and the paired normal tissues from 43 resection specimens. TGFβR Ⅰ expression was studied by immunohistochemistry, and the TGFβR Ⅰ gene was examined by polymerase chain reaction-single strand conformation polymorphism analysis (PCR-SSCP). The results obtained in this study demonstrated loss or reduction of TGFβR Ⅰ expression in 16 (37.2%) of the 43 tumor tissues. However, no somatic mutation other than a polymorphism was identified. The present study suggested that reduced TGFβR Ⅰ expression could contribute to the development of malignant phenotype of NSCLC, eventhough the genetic mutation of the TGFβR Ⅰ gene is not involved in the tumorigenesis of NSCLC and does not appear to be directly responsible for reduced expression of TGFβR Ⅰ.