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CD13-positive bone marrow-derived myeloid cells promote angiogenesis, tumor growth, and metastasis

Significance The progression of many solid tumors is associated with increased vascularization. We previously recognized involvement in tumor development and angiogenesis of tumor stromal cells expressing the CD13 protease aminopeptidase. The basic biological concept of participation of nontumor cells in the cancer stroma microenvironment is strengthened in the present study by our finding that a CD11b+CD13+ myeloid subset of bone marrow-derived cells affects pericyte biology and angiogenesis and thereby influences tumor growth and metastasis. Therapeutic implications of the identification of specific CD11+CD13+ myeloid bone marrow-derived cells as participants in the mechanism of tumor angiogenesis merit further investigation. Angiogenesis is fundamental to tumorigenesis and an attractive target for therapeutic intervention against cancer. We have recently demonstrated that CD13 (aminopeptidase N) expressed by nonmalignant host cells of unspecified types regulate tumor blood vessel development. Here, we compare CD13 wild-type and null bone marrow-transplanted tumor-bearing mice to show that host CD13+ bone marrow-derived cells promote cancer progression via their effect on angiogenesis. Furthermore, we have identified CD11b+CD13+ myeloid cells as the immune subpopulation directly regulating tumor blood vessel development. Finally, we show that these cells are specifically localized within the tumor microenvironment and produce proangiogenic soluble factors. Thus, CD11b+CD13+ myeloid cells constitute a population of bone marrow-derived cells that promote tumor progression and metastasis and are potential candidates for the development of targeted antiangiogenic drugs.