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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: J Pathol. 2013 Mar 14;230(1):82–94. doi: 10.1002/path.4171

Figure 7. Proposed model for the mechanisms underlying upregulation of iNOS protein expression in NPM-ALK+ T-cell lymphoma.

Figure 7

Under physiological conditions in T lymphocytes (purple), miR-26a is transcribed, processed, and then functions to inhibit the translation of iNOS mRNA to iNOS protein. In NPM-ALK+ T-cell lymphoma, NPM-ALK activates STAT3 by phosphorylation. Thereafter, pSTAT3 translocates to the nucleus where it suppresses transcription of MIR26A1. Decreased miR-26a levels in the cytoplasm allow translation of iNOS mRNA to iNOS protein. Dotted arrows indicate translocation to the nucleus or the cytoplasm. The lower panel details that pSTAT3 binds to the CTDSPL gene promoter at two sites, S1 and S2, to inhibit transcription. In addition, pSTAT3 inhibits transcription of MIR26A1, which is located in the intron of the CTDSPL gene.