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To elucidate the mechanism of glucocorticoid-induced metastases and growth inhibition of mouse teratocarcinoma OTT6050, syngeneic 129/Sv-CP+SlJ mice were subcutaneously (s.c.) injected with the tumor and treated with daily intraperitoneal (i.p.) injections of hydrocortisone in doses of 1.5 to 12.5 mg per mouse. The number of lymph-node and visceral metastases was greatly increased by the treatment with hydrocortisone unrelated to the doses and sexes. Tumor growth (the products of three principal diameters) of lymph-node metastases was dose-dependently inhibited by the treatment. Histologically, lymph-node metastatic tumors contained large masses of well-differentiated tissues compared with the s.c. transplanted tumor of the same size. The glucocorticoid receptors were measured using dextran-coated charcoal adsorption techniques with [3H] hydrocortisone. Glucocorticoid receptor contents were higher in lymph-node metastatic tumor (100 fmole/mg cytoplasmic protein, mean) than in s.c. transplanted tumors (74.5 fmole/mg, mean) respectively treated with 12.5 mg of hydrocortisone. The metastatic growth inhibition by hydrocortisone might be closely related to the receptor-mediated mechanisms and histological differentiation.

Metastatic enhancement and growth inhibition by glucocorticoid and its receptors in mouse teratocarcinoma OTT6050 in vivo.