Gene interactions and pathways from curated databases and text-mining

◀ Back to STAT3

ALK — STAT3

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: STAT3 → ALK (directlyIncreases, STAT3 Activity)
    Evidence: 9083098;11429593;9582023;15592455;12244095;14551213;11850821;9305919

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

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) : Anaplastic lymphoma kinase (ALK) activates Stat3 and protects hematopoietic cells from cell death ... We show here that expression of activated ALK induces the constitutive phosphorylation of Stat3 in transfected cells as well as in primary human ALCLs ... 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
Khoury et al., Clin Cancer Res 2003 (Lymphoma, Large B-Cell, Diffuse) : STAT3 activation correlates with but is not strictly dependent on ALK expression in ALCL
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
Cho-Vega et al., Leukemia 2004 (Lymphoma, Large-Cell, Anaplastic) : As SOCS3 is induced by activated signal transducer and activator of transcription 3 ( STAT3 ), and ALK activates STAT3 , we hypothesized that SOCS3 may play a role in ALK+ ALCL pathogenesis via the Janus kinase 3 (JAK3)-STAT3 pathway
Rust et al., J Clin Pathol 2005 (Lymphoma, Large B-Cell, Diffuse) : The high frequency of Mcl-1, Bcl-2, and Bcl-X ( L ) positive ALCL cases in the ALK- group compared with the ALK+ group indicates that ALK induced STAT3 activation is not the main regulatory pathway in ALCL
Moog-Lutz et al., J Biol Chem 2005 (MAP Kinase Signaling System) : We further showed for the first time that activation of ALK also resulted in a specific activation of STAT3
Rust et al., J Pathol 2005 (Lymphoma, Large B-Cell, Diffuse) : Lack of TIMP-1 expression in the tumour cells of ALK positive ALCLs argues against a direct role for ALK induced activation of STAT3 in the regulation of TIMP-1 expression in ALCL
Marzec et al., Lab Invest 2005 (Lymphoma, T-Cell) : Inhibition of ALK enzymatic activity in T-cell lymphoma cells induces apoptosis and suppresses proliferation and STAT3 phosphorylation independently of Jak3 ... 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
Takezawa et al., Clin Cancer Res 2011 (Cell Transformation, Neoplastic...) : Role of ERK-BIM and STAT3-survivin signaling pathways in ALK inhibitor induced apoptosis in EML4-ALK positive lung cancer ... Forced expression of EML4-ALK induced marked activation of extracellular signal regulated kinase ( ERK ) and STAT3 , but not that of AKT
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