ArticleAmerican journal of translational research2026
METTL16 promotes PD-L1 expression and mediates immunosuppression in B-cell lymphomas via m
Article in American journal of translational research, 2026. 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
objectivesImmune Checkpoint Inhibitors (ICIs) have changed cancer treatment. Altered expression of methyltransferase-like 16 (METTL16), one of the initial m
methodsOverexpression and knockdown strategies were used to regulate METTL16 expression in BCL cells, and then qPCR and western blot were employed to measure the levels of METTL16 and programmed death ligand 1 (PD-L1). A BCL-T cell co-culture system was employed to study immune evasion. T cell activation and infiltration into tumor and spleen tissues were assessed by flow cytometry. METTL16 function in regulating the m
resultsSilencing METTL16 in BCL cells inhibited their proliferation and reduced neoplastic expansion in vivo. METTL16 silencing enhanced T cell activation and cytokine release. METTL16 promoted the association of Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and PD-L1 mRNA by regulating m
conclusionOur findings indicate that METTL16 promotes BCL progression and immune evasion through epigenetic regulation of the PD-L1/PD-1 pathway.
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