CRIP1 involves the pathogenesis of multiple myeloma via dual-regulation of proteasome and autophagy
Multiple myeloma (MM) is an incurable hematological malignancy of plasma cells. The maintenance of protein homeostasis is critical for the survival of MM cells. The excess paraprotein in MM cells undergoes clearance through proteasomes or lysosomes, two inter-connected yet independent pathways. While proteasome inhibitors (PIs) serve as fundamental agents significantly improving patient outcomes, heightened autophagy activity diminishes sensitivity to PI treatment.Elevated CRIP1 levels serve as a biomarker for relapsed/refractory MM and correlate with shorter overall patient survival. To further comprehend the role of CRIP1 in multiple myeloma pathogenesis, we conducted transcriptome sequencing. Overall design: To investigate the role of CRIP1 in multiple myeloma pathogenesis, we generated multiple myeloma cells with CRIP1 knockdown by transfecting them with CRIP1-shRNA, utilizing Scramble-shRNA as a control. RNA sequencing was performed on both KMS11-CRIP1-sh and KMS11-Scr (control) cell lines, each replicated three times for biological validation.