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

Authors: Ahmed, Nuzhat  Riley, Clyde  Oliva, Karen  Stutt, Emma  Rice, Greg E  Quinn, Michael A 
Citation: Ahmed N, etal., J Pathol. 2003 Oct;201(2):229-37.
Pubmed: (View Article at PubMed) PMID:14517840
DOI: Full-text: DOI:10.1002/path.1441

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.

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CRRD Object Information
CRRD ID: 13441558
Created: 2017-10-27
Species: All species
Last Modified: 2017-10-27
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.