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The role of the tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase (IDO1), in tumor escape and metastasis formation was analyzed using two pairs of  Ido1+  and  Ido1−  murine breast cancer cell lines.  Ido1  expression in 4T1 cells was knocked down by shRNA, and  Ido1  expression in NT-5 cells was upregulated by stable transfection. Growth of  Ido1−  tumors and spontaneous metastasis formation were inhibited in immunocompetent mice. A higher level of cytotoxic T lymphocytes was generated by spleen cells from mice bearing  Ido1−  tumors than  Ido1+  tumors. Tumor and metastatic growth was enhanced in immunodeficient mice, confirming an intensified immune response in the absence of  Ido1  expression. However,  Ido1+  tumors grow faster than  Ido1−  tumors in immunodeficient SCID/beige mice (lacking T, B, and NK cells) suggesting that some  Ido1 -controlled nonimmunological mechanisms may be involved in tumor cell growth regulation.  In vitro  experiments demonstrated that downregulation of  Ido1  in tumor cells was associated with decreased cell proliferation, increased apoptosis, and changed expression of cell cycle regulatory genes, whereas upregulation of  Ido1  in the cells had the opposite effects. Taken together, our findings indicate that  Ido1  expression could exert immunological and nonimmunological effects in murine breast tumor cells.

Immunological and Nonimmunological Effects of Indoleamine 2,3-Dioxygenase on Breast Tumor Growth and Spontaneous Metastasis Formation