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DEK regulates B-cell proliferative capacity and is associated with aggressive disease in low-grade B-cell lymphomas.

Authors :
Hopper MA
Dropik AR
Walker JS
Novak JP
Laverty MS
Manske MK
Wu X
Wenzl K
Krull JE
Sarangi V
Maurer MJ
Yang ZZ
Del Busso MD
Habermann TM
Link BK
Rimsza LM
Witzig TE
Ansell SM
Cerhan JR
Jevremovic D
Novak AJ
Source :
Blood cancer journal [Blood Cancer J] 2024 Oct 09; Vol. 14 (1), pp. 172. Date of Electronic Publication: 2024 Oct 09.
Publication Year :
2024

Abstract

This study sheds light on the pivotal role of the oncoprotein DEK in B-cell lymphoma. We reveal DEK expression correlates with increased tumor proliferation and inferior overall survival in cases diagnosed with low-grade B-cell lymphoma (LGBCL). We also found significant correlation between DEK expression and copy number alterations in LGBCL tumors, highlighting a novel mechanism of LGBCL pathogenesis that warrants additional exploration. To interrogate the mechanistic role of DEK in B-cell lymphoma, we generated a DEK knockout cell line model, which demonstrated DEK depletion caused reduced proliferation and altered expression of key cell cycle and apoptosis-related proteins, including Bcl-2, Bcl-xL, and p53. Notably, DEK depleted cells showed increased sensitivity to apoptosis-inducing agents, including venetoclax and staurosporine, which underscores the therapeutic potential of targeting DEK in B-cell lymphomas. Overall, our study contributes to a better understanding of DEK's role as an oncoprotein in B-cell lymphomas, highlighting its potential as both a promising therapeutic target and a novel biomarker for aggressive LGBCL. Further research elucidating the molecular mechanisms underlying DEK-mediated tumorigenesis could pave the way for improved treatment strategies and better clinical outcomes for patients with B-cell lymphoma.<br /> (© 2024. The Author(s).)

Details

Language :
English
ISSN :
2044-5385
Volume :
14
Issue :
1
Database :
MEDLINE
Journal :
Blood cancer journal
Publication Type :
Academic Journal
Accession number :
39384745
Full Text :
https://doi.org/10.1038/s41408-024-01145-0