BRMS1 suppresses the PI3K/AKT/mTOR pathway to regulate autophagy in multiple myeloma

This study investigates the role of breast cancer metastasis suppressor 1 (BRMS1) in multiple myeloma (MM) progression. BRMS1 expression was significantly reduced in MM patient samples and cell lines. Functional assays revealed that BRMS1 overexpression suppressed MM cell proliferation, migration, and invasion while enhancing apoptosis and autophagic flux. Conversely, BRMS1 knockdown promoted tumorigenic behaviors. Pharmacological inhibition or activation of autophagy confirmed that BRMS1's tumor-suppressive effects are autophagy-dependent. Mechanistic studies demonstrated that BRMS1 regulates autophagy through the PI3K/AKT/mTOR signaling pathway. These findings establish BRMS1 as a potential tumor suppressor in MM, linking its function to autophagy and apoptosis regulation. Targeting BRMS1-mediated autophagy may provide a novel therapeutic approach for MM treatment and addressing disease progression. This study offers new insights into MM pathogenesis and potential strategies for improving patient outcomes.