| First Author | Jia W | Year | 2013 |
| Journal | Am J Pathol | Volume | 182 |
| Issue | 5 | Pages | 1821-31 |
| PubMed ID | 23499465 | Mgi Jnum | J:195339 |
| Mgi Id | MGI:5478647 | Doi | 10.1016/j.ajpath.2013.01.017 |
| Citation | Jia W, et al. (2013) Galectin-3 accelerates m2 macrophage infiltration and angiogenesis in tumors. Am J Pathol 182(5):1821-31 |
| abstractText | It is widely accepted that robust invasion of tumor-associated macrophages resembling M2 macrophage correlates with disease aggressiveness by affecting cancer cell invasion, metastasis, and angiogenesis. Many chemokines that induce migration of macrophages have been identified during inflammatory responses; however, further precise analysis of macrophage migration in the tumor microenvironment is required. Here, we analyzed the function of galectin-3 (Gal-3; gene LGALS3, alias Gal3) for macrophage chemotaxis using Gal3(-/-) mice as hosts, and a tumor allograft model. We engineered a concentration gradient of Gal-3 produced by the tumor. In this model, we found that macrophage infiltration was enhanced in tumors developing in these Gal3(-/-) mice relative to the Gal3(+/+) animals. This was accompanied by enhanced tumor angiogenesis and tumor growth in Gal3(-/-) mice. We found that macrophages of the M2 phenotype were dominant in infiltrates in the Gal3(-/-) mice and that they expressed only low levels of Gal-3. Gal3 knockdown by siRNA in macrophages resulted in enhanced chemotaxis. These data suggest that M2-like macrophages migrate into the tumor along a Gal-3 gradient and that high-level Gal-3 expression in the tumor results in acceleration of angiogenesis and tumor growth. Therefore, Gal-3 could be a potential target for the development of new treatments to inhibit tumor growth. |
