SNHG29 Interacts with CYLD via Mitochondrial Ribosomal Proteins to Reverse Rituximab Resistance in DLBCL

DLBCL represents the most common aggressive lymphoma subtype in China, with RTX resistance correlating to poor treatment outcomes. Our previous work demonstrated that modulating CYLD phosphorylation reverses RTX resistance. Given the emerging role of lncRNAs in apoptotic regulation and chemoresistance, and CYLD-associated lncRNAs have been implicated in chemoresistance reversal across various solid malignancies, we hypothesized that lncRNA-mediated control of CYLD phosphorylation could mechanistically address RTX resistance in DLBCL.Using RTX-resistant DLBCL models, RNA sequencing, and in vitro/in vivo validation, we identify a novel lncRNA-driven mechanism to overcome RTX resistance, offering therapeutic potential to improve patient outcomes.