Suppr超能文献

整合素连接激酶的表达随卵巢肿瘤分级增加,并由腹膜肿瘤液维持。

Integrin-linked kinase expression increases with ovarian tumour grade and is sustained by peritoneal tumour fluid.

作者信息

Ahmed Nuzhat, Riley Clyde, Oliva Karen, Stutt Emma, Rice Greg E, Quinn Michael A

机构信息

Gynaecological Cancer Research Centre, The Department of Obstetrics and Gynaecology, Royal Women's Hospital, The University of Melbourne, Victoria, Australia.

出版信息

J Pathol. 2003 Oct;201(2):229-37. doi: 10.1002/path.1441.

Abstract

Integrin-linked kinase (ILK) is a serine threonine kinase, overexpression of which promotes tumour growth and invasion through deregulation of the cell cycle. This study demonstrates the relative expression of ILK in normal, benign, low-grade, and high-grade (borderline, grade I/II, and grade III) ovarian tumours of serous, mucinous, endometrioid, and clear cell types in order to assess its potential as a marker for epithelial ovarian cancer progression. Seventy-three specimens including ten normal, ten benign, 14 borderline, 17 grade I/II, and 22 grade III were evaluated by immunohistochemistry. Immunoreactive ILK was not detectable in normal ovarian surface epithelium. All 53 carcinomas studied were positive and the staining intensity correlated significantly with the grade of the tumour. Ovarian cancer cell lines had high expression of ILK, while immortalized normal ovarian surface epithelial cell lines (HOSE) showed low basal expression of ILK by western blotting. Peritoneal tumour fluid (PTF) upregulated ILK expression in ovarian cancer cell lines but had no effect on HOSE cells. PTF-induced up-regulation of ILK expression in ovarian cancer cell lines correlated with the activation of the downstream protein kinase B (PKB/Akt) pathway. Collectively, these data demonstrate that ILK expression increases with ovarian cancer progression and that soluble factors in PTF mediate sustained overexpression of ILK in ovarian cancer cells. Suppression of ILK expression may therefore represent a novel and an efficient mechanism for controlling ovarian tumour growth.

摘要

整合素连接激酶(ILK)是一种丝氨酸苏氨酸激酶,其过表达通过细胞周期失调促进肿瘤生长和侵袭。本研究展示了ILK在浆液性、黏液性、子宫内膜样和透明细胞型的正常、良性、低级别和高级别(交界性、I/II级和III级)卵巢肿瘤中的相对表达情况,以评估其作为上皮性卵巢癌进展标志物的潜力。通过免疫组织化学对73个标本进行了评估,其中包括10个正常标本、10个良性标本、14个交界性标本、17个I/II级标本和22个III级标本。在正常卵巢表面上皮中未检测到免疫反应性ILK。所研究的所有53例癌均呈阳性,且染色强度与肿瘤分级显著相关。卵巢癌细胞系中ILK表达较高,而永生化的正常卵巢表面上皮细胞系(HOSE)通过蛋白质印迹显示ILK的基础表达较低。腹水(PTF)上调了卵巢癌细胞系中ILK的表达,但对HOSE细胞没有影响。PTF诱导的卵巢癌细胞系中ILK表达上调与下游蛋白激酶B(PKB/Akt)途径的激活相关。总体而言,这些数据表明ILK表达随卵巢癌进展而增加,并且PTF中的可溶性因子介导了卵巢癌细胞中ILK的持续过表达。因此,抑制ILK表达可能代表一种控制卵巢肿瘤生长的新的有效机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验