Integrative Genomic and Functional Analysis Identifies MOB3B as a Candidate Tumor Suppressor and Prognostic Biomarker in Diffuse Large B-Cell Lymphoma
Seoyul Lee
The Hun School of Princeton, Princeton, United States
Publication date: July 10, 2026
The Hun School of Princeton, Princeton, United States
Publication date: July 10, 2026
DOI: http://doi.org/10.34614/JIYRC2026I04
ABSTRACT
Diffuse large B-cell lymphoma (DLBCL) is an aggressive disease characterized by significant genetic heterogeneity and a high rate of relapse. Despite clinical advances, the specific functional role of the putative tumor suppressor MOB3B in this context is unclear. This study investigates the clinical and functional impact of MOB3B in DLBCL, testing the hypothesis that MOB3B deletion promotes disease progression by impairing cell-cycle regulation. The cBioPortal is utilized for survival-stratified copy-number analysis to correlate MOB3B expression with clinical outcomes. Functionally, SU-DHL-4 cells underwent transient transfection to induce MOB3B overexpression, followed by RT-qPCR validation, automated cell counting through LUNA-FL, and flow cytometric cell-cycle analysis. Clinical data reveal that MOB3B deletion is significantly enriched in deceased patients. Transient MOB3B overexpression led to dose-dependent mRNA upregulation and a progressive reduction in viable cell numbers. This reduction is primarily mediated by a significant G0/G1 arrest. These findings suggest that MOB3B serves as a potential prognostic biomarker and therapeutic target in aggressive DLBCL.
Diffuse large B-cell lymphoma (DLBCL) is an aggressive disease characterized by significant genetic heterogeneity and a high rate of relapse. Despite clinical advances, the specific functional role of the putative tumor suppressor MOB3B in this context is unclear. This study investigates the clinical and functional impact of MOB3B in DLBCL, testing the hypothesis that MOB3B deletion promotes disease progression by impairing cell-cycle regulation. The cBioPortal is utilized for survival-stratified copy-number analysis to correlate MOB3B expression with clinical outcomes. Functionally, SU-DHL-4 cells underwent transient transfection to induce MOB3B overexpression, followed by RT-qPCR validation, automated cell counting through LUNA-FL, and flow cytometric cell-cycle analysis. Clinical data reveal that MOB3B deletion is significantly enriched in deceased patients. Transient MOB3B overexpression led to dose-dependent mRNA upregulation and a progressive reduction in viable cell numbers. This reduction is primarily mediated by a significant G0/G1 arrest. These findings suggest that MOB3B serves as a potential prognostic biomarker and therapeutic target in aggressive DLBCL.
