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Front Physiol. 2014 Mar 28;5:114. doi: 10.3389/fphys.2014.00114. eCollection 2014.

The role IL-1 in tumor-mediated angiogenesis.

Author information

1
The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and The Cancer Research Center, Ben-Gurion University of the Negev Beer-Sheva, Israel.

Abstract

Tumor angiogenesis is one of the hallmarks of tumor progression and is essential for invasiveness and metastasis. Myeloid inflammatory cells, such as immature myeloid precursor cells, also termed myeloid-derived suppressor cells (MDSCs), neutrophils, and monocytes/macrophages, are recruited to the tumor microenvironment by factors released by the malignant cells that are subsequently "educated" in situ to acquire a pro-invasive, pro-angiogenic, and immunosuppressive phenotype. The proximity of myeloid cells to endothelial cells (ECs) lining blood vessels suggests that they play an important role in the angiogenic response, possibly by secreting a network of cytokines/chemokines and inflammatory mediators, as well as via activation of ECs for proliferation and secretion of pro-angiogenic factors. Interleukin-1 (IL-1) is an "alarm," upstream, pro-inflammatory cytokine that is generated primarily by myeloid cells. IL-1 initiates and propagates inflammation, mainly by inducing a local cytokine network and enhancing inflammatory cell infiltration to affected sites and by augmenting adhesion molecule expression on ECs and leukocytes. Pro-inflammatory mediators were recently shown to play an important role in tumor-mediated angiogenesis and blocking their function may suppress tumor progression. In this review, we summarize the interactions between IL-1 and other pro-angiogenic factors during normal and pathological conditions. In addition, the feasibility of IL-1 neutralization approaches for anti-cancer therapy is discussed.

KEYWORDS:

IL-1α; IL-1β; VEGF; VEGFR1; VEGFR2; angiogenesis; inflammation; myeloid cells

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