Experimental study on the effect of surmin on penile squamous carcinoma cell line(CUPE-1).
- Author:
Il Kyu KANG
1
;
Woo Chul MOON
Author Information
1. Department of Urology, College of Medicine, Chung-Ang University, Seoul, Korea.
- Publication Type:Clinical Trial ; In Vitro ; Original Article
- Keywords:
Penile Squamous carcinoma cell line(CUPE-1);
Suramin
- MeSH:
Animals;
Carcinoma, Squamous Cell*;
Epidermal Growth Factor;
Mice;
Mice, Nude;
Neoplasm Metastasis;
Robenidine;
Suramin
- From:Korean Journal of Urology
1993;34(5):748-763
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Experimental study was done to investigate the effect of suramin on the in vitro and in vivo proliferation and metastasis of penile squamous carcinoma cell line(CUPE-1), morphological changes of CUPE-1 cells induced by suramin and mechanism of action of suramin. Suramin inhibited in vitro proliferation of CUPE-1 significantly with 1C50 of 100 microgram/ml media. In vitro antiproliferative effect of suramin on CUPE-1 was reversible after stopping administration of the drug. Weekly intraperitoneal administration of 200 mg/kg of suramin to nude mouse inhibited the proliferation and metastasis of intraperitoneally implanted CUPE-1 cells significantly. but did not show significant effect on the proliferation of subcutaneously implanted CUPE-1 cells. Suramin induced senile changes on ultrastructure of CUPE-1 cells. Suramin of 300 microgram/ml inhibited the prolireration-stimulating effect of EGF significantly, whereas, suramin of 100 microgram/ml did not inhibit the effect of EGF significantly. Suramin did not show significant cytotoxicity on 3H-thymidine release assay. These results suggest that suramin is a promising drug for the treatment of advanced penile squamous cell carcinoma and blood level of suramin in clinical trial should be continuously maintained in about 300 microgram/ml, and that the main machanism of suramin against CUPE-1 is cytostatic. by antagonizing the action of EGF and inducing growth arrest and senile change.