Bone marrow derived mesenchymal stromal cells (MSCs) have recently been implicated as one source of the
tumor-associated stroma, which plays essential role in regulating
tumor progression. In spite of the intensive research, the individual factors in MSCs controlling
tumor progression have not been adequately defined. In the present study we have examined the role of
galectin-1 (Gal-1), a
protein highly expressed in
tumors with poor prognosis, in MSCs in the course of
tumor development. Co-
transplantation of wild type MSCs with 4T1 mouse
breast carcinoma cells enhances the incidence of palpable
tumors, growth, vascularization and
metastasis. It also reduces survival compared to animals treated with
tumor cells alone or in combination with
Gal-1 knockout MSCs. In vitro studies show that the absence of
Gal-1 in MSCs does not affect the number of migrating MSCs toward the
tumor cells, which is supported by the in vivo migration of intravenously injected MSCs into the
tumor. Moreover, differentiation of endothelial cells into blood vessel-like structures strongly depends on the expression of
Gal-1 in MSCs. Vital role of
Gal-1 in MSCs has been further verified in
Gal-1 knockout mice. By administering B16F10
melanoma cells into
Gal-1 deficient animals,
tumor growth is highly reduced compared to wild type animals. Nevertheless, co-injection of wild type but not
Gal-1 deficient MSCs results in dramatic
tumor growth and development.These results confirm that
galectin-1 is one of the critical factors in MSCs regulating
tumor progression.