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Tumor Prevention and Antitumor Immunity with Heat Shock Protein 70 Induced by 15-Deoxy-^12,14-prostaglandin J₂ in Transgenic Adenocarcinoma of Mouse Prostate Cells¹

Departments of Urology [D. K. V., C. Y. F. Y.] and Immunology [M. E. G., E. C.], Mayo Clinic/Foundation, Rochester, Minnesota 55905

The biological modifier ¹²-prostaglandin J₂ and related prostaglandins have been reported to have significant growth-inhibitory activity with induction of heat shock proteins (Hsps). Tumor-derived Hsps have been shown previously to elicit specific immunity to tumors from which they are isolated. In this study, 15-deoxy-^12,14-prostaglandin J₂ (15d-PGJ₂)-induced Hsp70 was purified from transgenic adenocarcinoma mouse prostate cells (TRAMP-C2). It was then tested for its ability to activate specific CTLs and induce protective immunity against prostate cancer in C57BL/6 mice. Treatment of cells with 8.0 µM 15d-PGJ₂ for 24 h caused significant induction of Hsp70 expression. The yield of Hsp70 purified from 15d-PGJ₂-treated cells was 4–5-fold higher when compared with untreated TRAMP-C2 cells. Vaccination of mice with Hsps isolated from TRAMP-C2 cells elicited tumor-specific CTLs and prevented the growth of TRAMP-C2 tumors. These results indicate that the induced heat shock proteins may have promising applications for antitumor, T-cell immunotherapy. In particular, these findings have important implications for the development of novel anticancer therapies aimed at promoting an immune response to prostate tumors.

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