The HGF/c-MET system is de-regulated in several human cancers, even if really few data are available on its expression and role in Testicular Germ Cell Tumors (TGCTs). Recently, we demonstrated that c-MET is expressed in tissue samples obtained from patients with different TGCTs and in three different cell lines representative of seminoma and non-seminoma TGCTs [1]. However, NT2D1, a non-seminoma cell line, revealed the greatest response to HGF treatment in terms of cell proliferation, migration and invasion. In this study we evaluated the role of PI3K in the HGF-dependent migration and invasion responses of NT2D1. To this aim, we stimulated with HGF the NT2D1 cells cultured with or without the PI3K inhibitor LY294002. Our results demonstrate that PI3K is involved in HGF-dependent NT2D1 migration and invasion, since PI3K inhibition abrogates the response to HGF. However, it is worth mentioning that the invasive capability of NT2D1 significantly increases administering the LY294002 alone, suggesting that PI3K adaptor protein, in this cell line, has also an anti-invasive role when recruited in c-MET-independent pathways. Further investigation is needed to understand the complex role of PI3K in NT2D1 invasive behavior.
PI3K role in the c-Met-mediated migrating and invading behavior of NT2D1 non-seminoma cells / Leonetti, Erica; Gesualdi, Luisa; Dinicola, Simona; Masiello, MARIA GRAZIA; Bizzarri, Mariano; Cucina, Alessandra; Catizone, Angiolina; Ricci, Giulia. - (2018). (Intervento presentato al convegno XV FISV Congress tenutosi a Sapienza University of Rome).
PI3K role in the c-Met-mediated migrating and invading behavior of NT2D1 non-seminoma cells
Erica Leonetti;Luisa Gesualdi;Simona Dinicola;Maria Grazia Masiello;Mariano Bizzarri;Alessandra Cucina;Angela Catizone;Giulia Ricci
2018
Abstract
The HGF/c-MET system is de-regulated in several human cancers, even if really few data are available on its expression and role in Testicular Germ Cell Tumors (TGCTs). Recently, we demonstrated that c-MET is expressed in tissue samples obtained from patients with different TGCTs and in three different cell lines representative of seminoma and non-seminoma TGCTs [1]. However, NT2D1, a non-seminoma cell line, revealed the greatest response to HGF treatment in terms of cell proliferation, migration and invasion. In this study we evaluated the role of PI3K in the HGF-dependent migration and invasion responses of NT2D1. To this aim, we stimulated with HGF the NT2D1 cells cultured with or without the PI3K inhibitor LY294002. Our results demonstrate that PI3K is involved in HGF-dependent NT2D1 migration and invasion, since PI3K inhibition abrogates the response to HGF. However, it is worth mentioning that the invasive capability of NT2D1 significantly increases administering the LY294002 alone, suggesting that PI3K adaptor protein, in this cell line, has also an anti-invasive role when recruited in c-MET-independent pathways. Further investigation is needed to understand the complex role of PI3K in NT2D1 invasive behavior.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
