Tumorigenesis disrupts hormonal regulation of tenascin expression in regressing dunning R 3327 H prostate carcinoma

We recently reported that androgen ablation either by orchiectomy or antiandrogen treatment resulted in the expression of the extracellular matrix glycoprotein tenascin in the regressing rat prostate. With the study presented here we investigated whether tenascin is expressed in the Dunning R 3327 H tumor and if orchiectomy and antiandrogen treatment affect tenascin expression. Experimentally, male rats were inoculated s.c. with pieces of Dunning tumor into the hind limb of both sides. Three months after inoculation rats were either orchiectomized or received a daily dose of 3 mg of cyproterone acetate or flutamide. Following a treatment period of 13 weeks, orchiectomy reduced tumor area by more than 60% compared to untreated controls. Cyproterone acetate and flutamide reduced tumor area significantly up to 30%. The amount and intensity of tenascin immunoreactivity appeared to be independent of the hormonal treatment and rather correlated to the content of tumor stroma. Those tumors with small, densely packed glandular ducts possessing almost no stromal tissue stained weakly for tenascin, whereas those tumors with larger ducts and significant stroma stained intensely. Staining intensity was particularly high at these sites where tumors infiltrated neighboring tissues, in proximity of infiltrating blood cells and close to necrotic areas. In summary, our results demonstrate a specific pattern of tenascin expression in Dunning R 3327 H rat prostate carcinomas, which appear to be independent of the hormonal treatment. We therefore conclude that tumorigenesis disrupts hormonal regulation of tenascin expression which we detected in the normal prostate gland after treatment with antiandrogens.