Over-expression of urokinase receptor in human epidermoid-carcinoma cell line (HEp3) increases tumorigenicity on chorio-allantoic membrane and in severe-combined-immunodeficient mice

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Title
Over-expression of urokinase receptor in human epidermoid-carcinoma cell line (HEp3) increases tumorigenicity on chorio-allantoic membrane and in severe-combined-immunodeficient mice
Author(s)
Mi Ae Lyu; Yang Kyu Choi; Bo Na Park; Byung Joo Park; Bum Joon Kim; Il Kyoo Park; Byung Hwa Hyun; Yoon Hoh Kook
Bibliographic Citation
International Journal of Cancer, vol. 77, pp. 257-263
Publication Year
1998
Abstract
Using chorio-allantoic membranes (CAMs) of chick embryos and severe- combined-immunodeficient (SCID) mice, we investigated the effects of urokinase-type plasminogen-activator receptor (u-PAR) over-expression on the process of invasion and tumorigenicity. By the transfection of u-PAR cDNA, 3 u-PAR-over-expressing clones expressing 1.6- to 4.6-fold more u-PAR mRNA than parent cells were obtained from a human epidermoid-carcinoma cell line, HEp3, that expresses urokinase-type plasminogen activator (u-PA) and u-PAR. All the u-PAR-over-expressing clones showed greater invasiveness (13 to 29%) than that of parent HEp3 cells on CAMs. Immunohistochemistry revealed densely stained u-PAR-positive cells near the margin of the tumor, where a u-PAR- over-expressing clone, designated SM-3, was invading thickened fibrous tissue on CAMs. Three u-PAR-over-expressing clones formed larger tumors (>40 mm3) than did parent HEp3 cells on CAMs. Moreover, when the u-PAR-over-expressing clone (SM-3) was injected s.c. into the back of the SCID mice it produced a larger tumor volume than the control (HEp3) and down-regulated (AS-2) clones and significantly shortened the survival of SCID mice. These results demonstrate that increased u-PAR expression is an important factor in determining the malignant phenotype that makes cancer cells more invasive and tumorigenic.
ISSN
0020-7136
Publisher
Wiley
DOI
http://dx.doi.org/10.1002/(SICI)1097-0215(19980717)77:2<257::AID-IJC15>3.0.CO;2-8
Type
Article
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1. Journal Articles > Journal Articles
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