Protumorigenic galectins 1 and 3 are upregulated in the liver of mice with growth hormone deficient action

DE LA FUENTE S; BACIGALUPO ML; SARRIAS L; GARCÍA LR; SOTELO AI ; BARTKE A; TRONCOSO MF; MIQUET JG

Mar del Plata

Congreso; LXVIII Reunión anual de la Sociedad Argentina de Investigaciones Clínicas (SAIC); 2023

Sociedad Argentina de Investigaciones Clínicas

Studies in humans and animals revealed a link between growth hormone (GH) and cancer risk. Transgenic mice overexpressing GH (GH-Tg) exhibit increased incidence of spontaneous and carcinogen-induced hepatocellular carcinoma. Galectins (GAL) 1 and 3 are involved in liver tumorigenesis in humans. Their expression is very low in normal hepatocytes but increase in liver tumors. We previously found that GAL1 and GAL3 are upregulated in GH-Tg mice liver, suggesting that GH positively modulates the hepatic expression of these protumorigenic galectins. The aim of this study was to evaluate if mice deficient in GH action, either due to GH deficiency or to absence of GH receptor, exhibit alterations in GAL1 and GAL3 liver expression.Hepatic GAL1 and GAL3 were analyzed by immunoblotting and RT-qPCR in GH receptor knockout (GHR-KO) mice, and in Ames dwarf mice deficient in GH, prolactin and thyroid-stimulating hormone. Young adult mice (2-3 months old) were used, normal littermates served as controls. Female and male mice were analyzed in independent experiments. Statistical analysis was performed by unpaired Student´s t-test (P