Regulation of stress tolerance by CREB1 sustains multiple myeloma cell survival.

ABSTRACT: Multiple myeloma (MM) cells originate from antibody-producing plasma cells and endure chronic oxidative and proteotoxic stress due to the excessive production of immunoglobulins and free light chains. We previously demonstrated that CD56 (also known as neuronal cell adhesion molecule 1) promotes cAMP-responsive element binding (CREB1) activation in MM cells to drive survival, without fully elucidating its mechanism of action. In this study, we describe the global role of CREB1 in regulating tolerance to cellular stresses in MM. Here, we present data to demonstrate that CREB1 directly or indirectly influences key proteins involved in the clearance of oxidants, the unfolded protein response (UPR), and autophagy. In silico data from real patients with MM showed that patients with high CREB1 e

SUBMITTER: Kudalkar R 

PROVIDER: S-EPMC12811356 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature