TGF-B signaling pathway is modulated by GPC3 in breast cancer cells

JAZMÍN MARTÍNEZ GÓMEZ; MARÍANGELES DÍAZ; MAGALÍ DELGADO PASTORE; ANA CLARA LUGONES; RAMIRO PERROTTA; STELLA MARIS RANUNCOLO; MARIANA SALATINO; PETERS, MARÍA GISELLE

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias; 2022

Sociedad Argentina de Investigación Clínica (SAIC), Sociedad Argentina de Inmunología (SAI); Sociedad ARgentina de Fisiología (SAFIS)

We have previously shown that GPC3, a downregulated proteoglycan in breast cancer, can induce a reversal of the epithelial-mesenchymal transition (EMT) traversed by mammary tumor cells. Through EMT modulation, GPC3 inhibits the metastatic spread. Since the TGF-β pathway is a key regulator of EMT, we set out to analyze whether the effects of GPC3 on tumor progression are mediated by this pathway.We performed in silico studies using the TCGA database. In association with the impact of GPC3 on EMT, gene enrichment analysis showed that the signatures involved in the EMT inhibition are upregulated in patients with high GPC3 expression levels (FDR