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NPM1 — STAT3

Text-mined interactions from Literome

Zhang et al., J Immunol 2002 (Lymphoma, T-Cell) : These data indicate that NPM/ALK activates STAT3 and that PP2A and lack of protein inhibitor of activated STAT3 may be important in maintaining STAT3 in the activated state in the ALK+ TCL cells
Zamo et al., Oncogene 2002 (Lymphoma, Large-Cell, Anaplastic) : Moreover, src family kinases are not necessary for NPM-ALK mediated Stat3 activation or transformation, suggesting that Stat3 may be phosphorylated directly by ALK
Amin et al., Oncogene 2003 (Lymphoma, Large B-Cell, Diffuse) : Our findings highlight the importance of JAK3 in activating STAT3 in ALCL, and that NPM-ALK mediated activation of STAT3 is influenced by the functional status of JAK3
Lai et al., Am J Pathol 2004 (Lymphoma, Large B-Cell, Diffuse) : As expected, TIMP1 positivity was higher in the ALK ( + ) group ( 15 of 19, 79 % ) compared with the ALK ( - ) group ( 5 of 24, 21 % ; P = 0.0002 ) because NPM-ALK restricted to ALK ( + ) tumors was previously shown to activate STAT3
Amin et al., Oncogene 2004 (Lymphoma, Large B-Cell, Diffuse) : It has been shown that NPM-ALK binds to and activates signal transducer and activator of transcription 3 ( STAT3 ) in vitro, and that STAT3 is constitutively active in ALK ( + ) ALCL cell lines and tumors
Marzec et al., Lab Invest 2005 (Lymphoma, T-Cell) : The inhibition of NPM/ALK activity resulted in malignant T cells in suppression of their growth, induction of apoptosis and inhibition of tyrosine phosphorylation of STAT3 , the key effector of the NPM/ALK induced oncogenesis
Honorat et al., Blood 2006 (Lymphoma, Large B-Cell, Diffuse) : Downregulation of SHP1 expression by RNAi in Karpas cells led to hyperphosphorylation of NPM-ALK , STAT3 activation , and increase in cell proliferation
Bard et al., Leukemia 2008 (Lymphoma, Large-Cell, Anaplastic...) : Nucleophosmin (NPM)-ALK, the characteristic fusion gene oncoprotein expressed in ALK ( + ) ALCL, directly contributes to the aberrant expression of IL-22R1, as transfection of NPM-ALK in Jurkat cells induced IL-22R1 expression and IL-22 mediated STAT3 activation
Marzec et al., Proc Natl Acad Sci U S A 2008 (Lymphoma, T-Cell) : Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 ( PD-L1, B7-H1 )
Ambrogio et al., Cancer Res 2009 (Lymphoma, Large-Cell, Anaplastic) : Finally, NPM-ALK increased the methylation of ZAP70 intron 1-exon 2 boundary region, and both NPM-ALK and STAT3 regulated the expression levels of DNA methyltransferase 1 in transformed T cells
Zhang et al., Proc Natl Acad Sci U S A 2011 : NPM-ALK acts through STAT3 , a transcription factor that binds to the IL-2R? gene promoter and enhances binding of DNA methyltransferases ( DNMTs ) to the promoter