Journal
BLOOD
Volume 125, Issue 6, Pages 981-991Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-04-568188
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Funding
- National Institutes of Health, National Cancer Institute [CA16672]
- National Institutes of Health, National Institute of General Medical Sciences [R01GM065899]
- National Institutes of Health, National Institute of Allergy and Infectious Diseases [R01AI050848]
- Center for Inflammation and Cancer of MD Anderson
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Diffuse large B-cell lymphoma (DLBCL) is an aggressive disease with a high proliferation rate. However, the molecular and genetic features that drive the aggressive clinical behavior of DLBCL are not fully defined. Here, we have demonstrated that activated Jun signaling is a frequent event in DLBCL that promotes dissemination of malignant cells. Downregulation of Jun dramatically reduces lymphoma cell adhesion to extracellular matrix proteins, subcutaneous tumor size in nude mice, and invasive behavior, including bone marrow infiltration and interaction with bone marrow stromal cells. Furthermore, using a combination of RNA interference and gene expression profiling, we identified Jun target genes that are associated with disseminated lymphoma. Among them, ITGAV, FoxC1, and CX3CR1 are significantly enriched in patients with 2 or more extranodal sites. Our results point to activated Jun signaling as a major driver of the aggressive phenotype of DLBCL.
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