Syntenin inhibition impairs stroma-tumor communication in multiple myeloma and improves bortezomib treatment efficiency.

ABSTRACT: Multiple myeloma (MM) remains incurable due to the development of drug resistance. We previously showed that communication between bone marrow stromal cells (BMSCs) and MM cells supports MM growth and triggers therapy resistance. This communication occurs through a plethora of mechanisms, including the release of cytokines and small extracellular vesicles (sEVs). The PDZ protein syntenin is a master regulator of intercellular communication, in particular via sEVs. In this study, we aimed to explore whether targeting syntenin, by genetic alteration or pharmacological inhibition, can disrupt BMSC-MM crosstalk, thereby rendering the MM cells more sensitive to therapy. We found that syntenin (SDCBP) is highly expressed in inflammatory BMSC of MM patients and that its expression in BM aspirates

SUBMITTER: Tu C 

PROVIDER: S-EPMC12358804 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature