Literature DB >> 10449805

STAT signaling in the pathogenesis and treatment of cancer.

D A Frank1.   

Abstract

Exceptional advances have been made recently in our understanding of the signaling pathways that control cellular growth, differentiation, and survival. These processes are regulated by extracellular stimuli such as cytokines, cell-cell interactions, and cell-matrix interactions, which trigger a series of intracellular events culminating in the modulation of specific genes. STATs are a highly homologous group of transcription factors that are activated by various pathways and regulate many of the genes controlling cellular function. STATs are activated by tyrosine phosphorylation and modulated by serine phosphorylation, placing them at a convergence point for numerous intracellular signaling pathways. Given the importance of STATs in the control of normal physiologic processes, it is not surprising that inappropriate activation of these proteins has been found in human malignancies. A number of distinct mechanisms have been elucidated by which STATs are activated inappropriately, including autocrine or paracrine stimulation of normal receptors and increased activity of tyrosine kinases through enhanced expression, mutations, or the presence of activating proteins. Furthermore, inappropriate STAT serine phosphorylation has been found in several tumors as well. The increased understanding of signaling pathways in tumors can be translated into therapeutic strategies that have the potential to be more selective and less toxic than current anti-cancer treatments. Approaches which may be effective include the development of antagonists of receptors that can trigger STAT activation, inhibitors of the tyrosine and serine kinases that phosphorylate and activate STATs, agents that decrease STAT levels or inhibit their recruitment to kinases, and molecules that can prevent the binding of STATs to target DNA sequences. Thus, elucidation of cellular and biochemical processes in tumors has enhanced our understanding of the pathogenesis of malignancies and may provide the basis for significant advances in therapy.

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Year:  1999        PMID: 10449805      PMCID: PMC2230445     

Source DB:  PubMed          Journal:  Mol Med        ISSN: 1076-1551            Impact factor:   6.354


  226 in total

Review 1.  Jaks and Stats in signaling by the cytokine receptor superfamily.

Authors:  J N Ihle; I M Kerr
Journal:  Trends Genet       Date:  1995-02       Impact factor: 11.639

2.  Choice of STATs and other substrates specified by modular tyrosine-based motifs in cytokine receptors.

Authors:  N Stahl; T J Farruggella; T G Boulton; Z Zhong; J E Darnell; G D Yancopoulos
Journal:  Science       Date:  1995-03-03       Impact factor: 47.728

3.  STAT proteins participate in the regulation of the vasoactive intestinal peptide gene by the ciliary neurotrophic factor family of cytokines.

Authors:  A Symes; S Lewis; L Corpus; P Rajan; S E Hyman; J S Fink
Journal:  Mol Endocrinol       Date:  1994-12

4.  Requirement of serine phosphorylation for formation of STAT-promoter complexes.

Authors:  X Zhang; J Blenis; H C Li; C Schindler; S Chen-Kiang
Journal:  Science       Date:  1995-03-31       Impact factor: 47.728

5.  The role of shared receptor motifs and common Stat proteins in the generation of cytokine pleiotropy and redundancy by IL-2, IL-4, IL-7, IL-13, and IL-15.

Authors:  J X Lin; T S Migone; M Tsang; M Friedmann; J A Weatherbee; L Zhou; A Yamauchi; E T Bloom; J Mietz; S John
Journal:  Immunity       Date:  1995-04       Impact factor: 31.745

6.  Identification and purification of human Stat proteins activated in response to interleukin-2.

Authors:  J Hou; U Schindler; W J Henzel; S C Wong; S L McKnight
Journal:  Immunity       Date:  1995-04       Impact factor: 31.745

7.  Serum interleukin-6 levels correlate with prognosis in diffuse large-cell lymphoma.

Authors:  J F Seymour; M Talpaz; F Cabanillas; M Wetzler; R Kurzrock
Journal:  J Clin Oncol       Date:  1995-03       Impact factor: 44.544

8.  An amino acid substitution in the Drosophila hopTum-l Jak kinase causes leukemia-like hematopoietic defects.

Authors:  H Luo; W P Hanratty; C R Dearolf
Journal:  EMBO J       Date:  1995-04-03       Impact factor: 11.598

9.  Prolactin, growth hormone, erythropoietin and granulocyte-macrophage colony stimulating factor induce MGF-Stat5 DNA binding activity.

Authors:  F Gouilleux; C Pallard; I Dusanter-Fourt; H Wakao; L A Haldosen; G Norstedt; D Levy; B Groner
Journal:  EMBO J       Date:  1995-05-01       Impact factor: 11.598

10.  Elevated levels of members of the STAT family of transcription factors in breast carcinoma nuclear extracts.

Authors:  C J Watson; W R Miller
Journal:  Br J Cancer       Date:  1995-04       Impact factor: 7.640

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  28 in total

1.  Nucleocytoplasmic translocation of Stat1 is regulated by a leucine-rich export signal in the coiled-coil domain.

Authors:  A Begitt; T Meyer; M van Rossum; U Vinkemeier
Journal:  Proc Natl Acad Sci U S A       Date:  2000-09-12       Impact factor: 11.205

2.  Leelamine mediates cancer cell death through inhibition of intracellular cholesterol transport.

Authors:  Omer F Kuzu; Raghavendra Gowda; Arati Sharma; Gavin P Robertson
Journal:  Mol Cancer Ther       Date:  2014-03-31       Impact factor: 6.261

3.  Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis.

Authors:  J A Cutler; R Tahir; S K Sreenivasamurthy; C Mitchell; S Renuse; R S Nirujogi; A H Patil; M Heydarian; X Wong; X Wu; T-C Huang; M-S Kim; K L Reddy; A Pandey
Journal:  Leukemia       Date:  2017-02-17       Impact factor: 11.528

4.  STAT1 Activation Is Enhanced by Cisplatin and Variably Affected by EGFR Inhibition in HNSCC Cells.

Authors:  Nicole C Schmitt; Sumita Trivedi; Robert L Ferris
Journal:  Mol Cancer Ther       Date:  2015-07-03       Impact factor: 6.261

5.  EGFR and KRAS mutations do not enrich for the activation of IL-6, JAK1 or phosphorylated STAT3 in resected lung adenocarcinoma.

Authors:  Timothy D Clay; Prudence A Russell; Hongdo Do; Vijaya Sundararajan; Matthew Conron; Gavin M Wright; Benjamin Solomon; Alexander Dobrovic; Sue-Anne McLachlan; Melissa M Moore
Journal:  Med Oncol       Date:  2017-09-06       Impact factor: 3.064

6.  ephrinB1 signals from the cell surface to the nucleus by recruitment of STAT3.

Authors:  Yong-Sik Bong; Hyun-Shik Lee; Laura Carim-Todd; Kathleen Mood; Tagvor G Nishanian; Lino Tessarollo; Ira O Daar
Journal:  Proc Natl Acad Sci U S A       Date:  2007-10-22       Impact factor: 11.205

7.  SARS-CoV pathogenesis is regulated by a STAT1 dependent but a type I, II and III interferon receptor independent mechanism.

Authors:  Matthew B Frieman; Jun Chen; Thomas E Morrison; Alan Whitmore; William Funkhouser; Jerrold M Ward; Elaine W Lamirande; Anjeanette Roberts; Mark Heise; Kanta Subbarao; Ralph S Baric
Journal:  PLoS Pathog       Date:  2010-04-08       Impact factor: 6.823

8.  MUC1 is a downstream target of STAT3 and regulates lung cancer cell survival and invasion.

Authors:  Jingchun Gao; Matthew J McConnell; Bin Yu; Jiannong Li; Justin M Balko; Esther P Black; Joseph O Johnson; Mark C Lloyd; Soner Altiok; Eric B Haura
Journal:  Int J Oncol       Date:  2009-08       Impact factor: 5.650

9.  Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation.

Authors:  Atsushi Hosui; Akiko Kimura; Daisuke Yamaji; Bing-mei Zhu; Risu Na; Lothar Hennighausen
Journal:  J Exp Med       Date:  2009-03-30       Impact factor: 14.307

10.  Avicin D: a protein reactive plant isoprenoid dephosphorylates Stat 3 by regulating both kinase and phosphatase activities.

Authors:  Valsala Haridas; Goshi Nishimura; Zhi-Xiang Xu; Fiona Connolly; Margaret Hanausek; Zbigniew Walaszek; Robert Zoltaszek; Jordan U Gutterman
Journal:  PLoS One       Date:  2009-05-18       Impact factor: 3.240

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