After emigration from the bone marrow into the peripheral blood, monocytes enter tissues and differentiate into macrophages. Monocytes/macrophages have many roles in immune regulation, angiogenesis, and tumor metastasis and invasion. In addition, studies have revealed that these cells are essential to tumor progression. Recently, an accumulation of evidence has indicated that macrophages in distinct regions of tumor masses have distinct origins. For instance, classical monocytes appear to be a major source of macrophages in tumor epithelial, perivascular, and hypoxic regions. In contrast, non-classical monocytes are an important source of macrophages in the tumor perivascular region. During the past century, it has been demonstrated that several chemoattractants can regulate the recruitment of monocytes/macrophages to tumor sites. Despite the importance of monocytes/macrophages in tumor progression, there had been, until recently, no efforts to summarize receptor-ligand pairs between tumor-derived chemokines and corresponding receptors in monocytes in different microenvironments. In this review, we present a cohesive view of the distinct expression patterns of chemokine receptors in two different monocyte subsets (classical and non-classical monocytes) and describe their roles in monocyte/macrophage recruitment into distinct tumor microenvironments. This review provides insight into the behavior of monocytes/macrophages in different tumor microenvironments.
|Number of pages||10|
|Journal||Biochimica et Biophysica Acta - Reviews on Cancer|
|Publication status||Published - 2013 Apr|
Bibliographical noteFunding Information:
This work was supported by grants from the National Research Foundation of Korea, funded by the Korean Government (Ministry of Education, Science, and Technology [MEST]) ( NRF-2011-355-E00020 ); the Korea Health 21 R&D Project, Ministry of Health Welfare & Family Affairs ( A085136 ); the Bio & Medical Technology Development program ( 2011-0019267 ); the National Nuclear R&D Program through the National Research Foundation of Korea (NRF) grant funded by the Korean Government (MEST) ( 2010-0018544 ); and the Basic Science Research Program ( 2012002916 ) of the National Research Foundation of Korea (NRF) funded by the Korean Government (MEST) .
All Science Journal Classification (ASJC) codes
- Cancer Research