Downregulation of stromal syntenin sustains AML development

• DOI: 10.15252/emmm.202317570
• Publication Date: 2023-10-12T05:36:27Z
• Authors: Raphael Leblanc; Rania Ghossoub; Armelle Goubard; Rémy Castellano; Joanna Fares; Luc Camoin; Stephane Audebert; Marielle Balzano; Berna Bou‐Tayeh; Cyril Fauriat; Norbert Vey; Sylvain Garciaz; Jean‐Paul Borg; Yves Collette; Michel Aurrand‐Lions; Guido David; Pascale Zimmermann
• Keywords: Crosstalk

Abstract The crosstalk between cancer and stromal cells plays a critical role in tumor progression. Syntenin is small scaffold protein involved the regulation of intercellular communication that emerging as target for therapy. Here, we show certain aggressive forms acute myeloid leukemia (AML) reduce expression syntenin bone marrow (BMSC). Stromal deficiency, turn, generates pro‐tumoral microenvironment. From serial transplantations mice co‐culture experiments, conclude syntenin‐deficient BMSC stimulate AML aggressiveness by promoting cell survival synthesis. This activity supported increased endoglin, classical marker BMSC, which trans stimulates translational activity. In short, our study reveals vicious signaling loop potentially at heart AML–stroma unsuspected tumor‐suppressive effects need to be considered during systemic targeting