期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 189, 期 4, 页码 900-910出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2018.12.005
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资金
- Japan Agency for Medical Research and Development [18cm0106508h0002, 18gm5010002s1102]
- Japan Society for the Promotion of Science [16H02470]
- Grants-in-Aid for Scientific Research [16H02470] Funding Source: KAKEN
Galectin-3 (Gal-3; gene LGALS3) is a member of the beta-galactose binding lectin family. Previous studies showed that Gal-3 is expressed in several tissues across species and functions as a regulator of cell proliferation, apoptosis, adhesion, and migration, thus affecting many aspects of events, such as angiogenesis and tumorigenesis. Although several reports have suggested that the level of Gal-3 expression correlates positively with tumor progression, herein we show that highly metastatic mouse melanoma B16/BL6 cells express less Gal-3 than B16 cells with a lower metastatic potential. It was found that overexpression of Gal-3 in melanoma cells in fact suppresses metastasis. In contrast, knocking out Gal-3 expression in cancer cells promoted cell aggregation mediated through interactions with platelets and fibrinogen in vitro and increased the number of metastatic foci in vivo. Thus, reduced Gal-3 expression results in the up-regulation of 03 integrin expression, and this contributes to metastatic potential. These findings indicate that changes of Gal-3 expression in cancer cells during tumor progression influence the characteristics of metastatic cells.
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