© 1995 by Oxford University Press
Journal of the National Cancer Institute, Vol. 87, No. 7, 506-516,
April 5, 1995
© 1995 Oxford University Press
Expression of Vascular Endothelial Growt Factor and Its Receptors fit and KDR in Ovarian Carcinoma
Reproductive Molecular Research Group, Department of Obstetrics and Gynaecology, University of Cambridge The Rosie Maternity Hospital, Cambridge, England
The Microchemical Facility, Babraham Institute Babraham, Cambridge.
MRC Clinical Oncology and Radio-therapeutics Unit, Medical Research Council Centre Cambridge
Correspondence to present address. Christine A. Boocock, Ph.D., Department of Dental Surgery and Periodontology, University of Dundee, Dundee, DD1, 4HN, Scotland.
BACKGROUND:: Two thirds of patients with ovarian carcinoma have advanced disease at diagnosis and have poor progenoses because of the presence of highly invasive carcinoma cells and rapidly accumulating ascitic fluid. Vascular endothelial growth factor (VEGF), a potent mitogen of endothelial cells, is produced in elevated amounts by many tumors, including ovarian carcinomas. The known human receptors for VEGF, fit and KDR, are both cell surface tyrosine kinases and are expressed predominantly on endothelial cells. Acting through these receptors, VEGF may stimulate angio-genesis and promote tumor progression. Purpose: We aimed to clarify the function of VEGF in tumor development by identifying the cells in ovarian carcinoma tissue that express VEGF and its receptors.
METHODS:: VEGF, fit, and KDR expression was localized by in situ hybridization and immunohistochemistry in frozen sections of primary tumors from five patients with ovarian carcinoma and from metastases of ovarian carcinoma from three different patients. Reverse transcription followed by polymerase chain reaction (RT-PCR) and an enzyme-linked immunosorbent assay were used to analyze VEGF, fit, and KDR expression in six epithelial cell lines derived from ovarian carcinoma ascites from five additional patients.
RESULTS:: Messenger RNAs (mRNAs) encoding VEGF, fit, and KDR were detected in primary ascitic cells and in three of four ovarian carcinoma cell lines examined by RT-PCR. Two novel complementary DNAs that may encode truncated, soluble forms of fit were cloned from one primary source. VEGF levels of 20–120 pAf were found in culture media conditioned by the cell lines. Elevated expression of VEGF mRNA was found in all primary tumors and metastases, especially at the margins of tumor acini. VEGF immunoreactivity was concentrated in clusters of tumor cells and patches of stromal matrix. fit immunoreactivity was confined to tumor blood vessels, but fit mRNA was not detected by in situ hybridization. In contrast, KDR mRNA was detected not only in vascular endothelial cells but also in tumor cells at primary malignant sites.
CONCLUSIONS:: VEGF is expressed by tumor cells in primary and metastatic ovarian carcinoma and accumulates in the stromal matrix. Its receptors, fit and KDR, are expressed by some tumor blood vessels; KDR is also expressed by some tumor cells that coexpress VEGF. This is the first localization of KDR expression in nonendothelial cells. Implications: Coexpression of VEGF and KDR by tumor cells in ovarian carcinoma raises the possibility of autocrine stimulation and of therapeutic strategies targeting this receptor-ligand interaction. (J Natl Cancer Inst 8706–516, 1995)
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