Identification of Galectin-1 as a Critical Factor in Function of Mouse Mesenchymal Stromal Cell-Mediated Tumor Promotion

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...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Szebeni Gábor
Kriston-Pál Éva
Blazsó Péter
Katona Róbert László
Novák Julianna
Szabó Enikő
Czibula Ágnes
Fajka-Boja Roberta
Hegyi Beáta
Uher Ferenc
Krenács László
Joó Gabriella
Monostori Éva
Dokumentumtípus: Cikk
Megjelent: 2012
Sorozat:PLOS ONE 7 No. 7
Tárgyszavak:
doi:10.1371/journal.pone.0041372

mtmt:2057717
Online Access:http://publicatio.bibl.u-szeged.hu/29426
Leíró adatok
Tartalmi kivonat: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.
Terjedelem/Fizikai jellemzők:13
ISSN:1932-6203