ArticleClinical and experimental medicine2025
Targeting SET to counteract Lyn activation demonstrates anti-cancer potential in diffuse large B-cell lymphoma.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diffuse large B-cell lymphoma (DLBCL) is characterized by molecular complexity and heterogeneity. The SET oncoprotein is overexpressed in B-cell chronic lymphocytic leukemia and non-Hodgkin lymphoma. Acting as an intrinsic inhibitor of the tumor suppressor protein phosphatase 2A (PP2A), targeting SET has shown anti-cancer activity. In this study, we investigated the molecular mechanism of SET antagonism in DLBCL. Overexpression of SET resulted in decreased phosphatase activities of PP2A and SHP-1, while activating Lyn. Conversely, SET inhibition, either through antagonists or siRNA, led to the activation of PP2A and SHP-1, resulting in the inactivation of Lyn. Analysis of public datasets revealed upregulation of Lyn in late-stage DLBCL samples, which was associated with a worse outcome. Ectopic expression of Lyn enhanced the cell viability and migratory capacity of DLBCL cells. Notably, Lyn inhibited PP2A and SHP-1 phosphatase activities, suggesting the existence of a SET/PP2A/SHP-1/Lyn feedback loop. Immunohistochemically, SHP-1 levels were negatively correlated with pLyn/Lyn levels in DLBCL tissues. Overall, these results suggest that SET antagonism to inactivate Lyn represents an attractive approach for DLBCL treatment.
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