Mechanism of the antitumor activity of 5,5'-bis(2'-tetrahydropyranyl) secalonic acid D against Meth-A.

The mechanism of the antitumor activity of 5,5'-bis(2'-tetrahydropyranyl) secalonic acid D (PSA) was examined in Balb/c mice bearing Meth-A fibrosarcoma. IP-injected PSA showed remarkable antitumor activity against IP-implanted Meth-A tumor. Antitumor activity of PSA was not abolished by treatment with silica as an antimacrophage agent or anti-asialo GM1 antiserum that selectively eliminates natural killer cells. Although it was significantly suppressed by treatment with antithymocyte globulin in Balb/c mice, PSA was effective against Meth-A tumors implanted in athymic Balb/c mice. PSA inhibited in vitro Meth-A proliferation as effectively as mitomycin C and was not effective against Meth-A tumor implanted SC at a site where direct contact of PSA and Meth-A cells was unlikely. These results suggest that the antitumor activity of PSA was mainly achieved by inhibiting Meth-A cell proliferation, although the host T cell-mediated immunity was partly involved in the eventual therapeutic efficacy of PSA.