Abstract
Abstract In the United States, breast cancer death is the second leading cause of cancer deaths in women, primarily due to the occurrence of metastatic disease. We have identified a potential novel therapeutic agent derived from an edible root of the plant Colocasia esculenta, commonly known as taro, which has significant antimetastatic activity in a preclinical model of metastatic breast cancer and that should have minimal toxicity. We have shown for the first time that a water-soluble extract of taro (TE) potently inhibits lung colonizing ability (95-99%) as well as spontaneous metastasis from mammary gland-implanted tumors (85%), in a murine model of highly metastatic ER, PR and Her-2/neu negative breast cancer. TE modestly inhibits the proliferation of some, but not all, breast and prostate cancer cell lines and also causes morphologic changes including cell rounding. TE inhibits prostaglandin E2 (PGE2) levels and because PGE2 is a potent immune modulator, we examined the role of immunity in the therapeutic response to TE. We first examined the effect of TE on Natural Killer (NK) cell activities. TE modestly increases NK-mediated tumor cell lysis in vitro. We determined the effect of NK depletion on TE efficacy in vivo. The ability of TE to inhibit metastasis was modestly compromised in NK-depleted mice indicating that NK cells play a minor role in TE-mediated antimetastatic activity. To examine the role of T and B lymphocytes, TE efficacy was examined in Balb/c SCID mice. Antimetastatic activity of TE was completely lost in SCID mice lacking mature T and B cells. Thus, T and /or B cell functions contribute to the mechanism by which TE inhibits metastasis. In published studies we have identified the active component of TE as one of three closely related taro proteins, tarin, taro lectin and 12-kDa storage protein. Current studies are determining how these candidate proteins affect immune functions to inhibit breast cancer metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3437. doi:1538-7445.AM2012-3437
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