Relevancia de galectina-1 en el carcinoma hepatocelular : su función como nexo entre los hepatocitos tumorales y el endotelio sinusoidal
Hepatocellular carcinoma (HCC) represents the third cause of cancer death worldwide. Galectin-1 (Gal1), a ?-galactoside-binding protein, is increased in HCC. Our group has previously shown that Gal1 promotes in vivo tumor growth and metastasis. The main objective of this Ph. D. Thesis consisted in i...
Guardado en:
| Autor principal: | |
|---|---|
| Otros Autores: | |
| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
| Publicado: |
Facultad de Farmacia y Bioquímica
2016
|
| Materias: | |
| Acceso en línea: | http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1178 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1178.dir/1178.PDF |
| Aporte de: |
| Sumario: | Hepatocellular carcinoma (HCC) represents the third cause of cancer death worldwide. Galectin-1 (Gal1), a ?-galactoside-binding protein, is increased in HCC. Our group has previously shown that Gal1 promotes in vivo tumor growth and metastasis. The main objective of this Ph. D. Thesis consisted in investigating the role of Gal1 in the interplay between tumor hepatocytes and endothelial sinusoidal cells within the HCC microenvironment.\nWe demonstrated that tumor hepatocyte-derived Gal1 induces SK-HEP-1 human liver sinusoidal endothelial cell (SEC) proliferation and migration. Moreover, Gal1 overexpression in HCC cells, partly induced by TGF-?1, promoted their adhesion to SK-HEP-1 SECs. Furthermore, we showed that Gal1 modulates HepG2 human HCC cell proliferation and sensitivity to TGF-?1-induced growth inhibition. Moreover, CD13 was identified as a novel Gal1 ligand in SK-HEP-1 cells.\nIn conclusion, our results indicate that Gal1 is relevant within the HCC microenvironment by contributing to tumor hepatocyte dissemination. These findings also highlight that Gal1 may be an interesting molecular target to design HCC therapeutic strategies. |
|---|