Fli-1

Summary

Gene Symbol: Fli-1
Description: Fli-1 proto-oncogene, ETS transcription factor
Alias: BDPLT21, EWSR2, SIC-1, Friend leukemia integration 1 transcription factor, Ewing sarcoma breakpoint region 2, Friend leukemia virus integration 1, transcription factor ERGB
Species: human
Products:     Fli-1

Top Publications

  1. Bhagirath T, Abe S, Nojima T, Yoshida M. Molecular analysis of a t(11;22) translocation junction in a case of Ewing's sarcoma. Genes Chromosomes Cancer. 1995;13:126-32 pubmed
    ..Instead, a palindromic hexamer 5'-GCTAGC-3' was found to flank the breakpoints of both genes on der(22), which may have a functional significance in the genesis of the t(11;22). ..
  2. Bujor A, Asano Y, Haines P, Lafyatis R, Trojanowska M. The c-Abl tyrosine kinase controls protein kinase C?-induced Fli-1 phosphorylation in human dermal fibroblasts. Arthritis Rheum. 2011;63:1729-37 pubmed publisher
    ..Thus, blocking the TGF?/c-Abl/PKC?/phospho-Fli-1 pathway could be an attractive alternative approach to therapy for scleroderma. ..
  3. Asano Y, Stawski L, Hant F, Highland K, Silver R, Szalai G, et al. Endothelial Fli1 deficiency impairs vascular homeostasis: a role in scleroderma vasculopathy. Am J Pathol. 2010;176:1983-98 pubmed publisher
    ..Importantly, vascular characteristics of Fli1 CKO mice are recapitulated by SSc microvasculature. Thus, persistently reduced levels of Fli1 in endothelial cells may play a critical role in the development of SSc vasculopathy. ..
  4. Ramakrishnan R, Fujimura Y, Zou J, Liu F, Lee L, Rao V, et al. Role of protein-protein interactions in the antiapoptotic function of EWS-Fli-1. Oncogene. 2004;23:7087-94 pubmed
    ..These results suggest that the ability of EWS-Fli-1/Fli-1 to target transcriptional cofactor(s) and modulate apoptotic pathways may be responsible for its antiapoptotic and tumorigenic activities. ..
  5. Barbeau B, Bergeron D, Beaulieu M, Nadjem Z, Rassart E. Characterization of the human and mouse Fli-1 promoter regions. Biochim Biophys Acta. 1996;1307:220-32 pubmed
    ..Constructions of the human homologue containing nearly 1.5 kbp of Fli-1 5' flanking region was also inactive in transfected cells. These results suggest that multiple levels of regulation might control the Fli-1 expression. ..
  6. Gascoyne D, Thomas G, Latchman D. The effects of Brn-3a on neuronal differentiation and apoptosis are differentially modulated by EWS and its oncogenic derivative EWS/Fli-1. Oncogene. 2004;23:3830-40 pubmed
    ..These data demonstrate that oncogenic rearrangement of EWS to produce EWS/Fli-1 may enhance the antiapoptotic effect of Brn-3a and inhibit its ability to promote neuronal differentiation. ..
  7. Kubo M, Czuwara Ladykowska J, Moussa O, Markiewicz M, Smith E, Silver R, et al. Persistent down-regulation of Fli1, a suppressor of collagen transcription, in fibrotic scleroderma skin. Am J Pathol. 2003;163:571-81 pubmed
    ..Persistent down-regulation of Fli1 in scleroderma fibroblasts in vivo may directly contribute to uncontrolled matrix deposition in scleroderma skin. ..
  8. Rekhtman N, Radparvar F, Evans T, Skoultchi A. Direct interaction of hematopoietic transcription factors PU.1 and GATA-1: functional antagonism in erythroid cells. Genes Dev. 1999;13:1398-411 pubmed
    ..1. Our results indicate that the stoichiometry of directly interacting but opposing transcription factors may be a crucial determinant governing processes of normal differentiation and malignant transformation. ..
  9. Eisbacher M, Holmes M, Newton A, Hogg P, Khachigian L, Crossley M, et al. Protein-protein interaction between Fli-1 and GATA-1 mediates synergistic expression of megakaryocyte-specific genes through cooperative DNA binding. Mol Cell Biol. 2003;23:3427-41 pubmed
    ..This work suggests that Fli-1 and GATA-1 work together to activate the expression of genes associated with the terminal differentiation of megakaryocytes. ..

More Information

Publications97

  1. Starck J, Cohet N, Gonnet C, Sarrazin S, Doubeikovskaia Z, Doubeikovski A, et al. Functional cross-antagonism between transcription factors FLI-1 and EKLF. Mol Cell Biol. 2003;23:1390-402 pubmed
  2. Sankar S, Bell R, Stephens B, Zhuo R, Sharma S, Bearss D, et al. Mechanism and relevance of EWS/FLI-mediated transcriptional repression in Ewing sarcoma. Oncogene. 2013;32:5089-100 pubmed publisher
  3. Owen L, Kowalewski A, Lessnick S. EWS/FLI mediates transcriptional repression via NKX2.2 during oncogenic transformation in Ewing's sarcoma. PLoS ONE. 2008;3:e1965 pubmed publisher
    ..2 binding. These data demonstrate that the transcriptional repressive function of NKX2.2 is necessary, and sufficient, for the oncogenic phenotype of Ewing's sarcoma, and suggest a therapeutic approach to this disease. ..
  4. Wang Y, Fan P, Kahaleh B. Association between enhanced type I collagen expression and epigenetic repression of the FLI1 gene in scleroderma fibroblasts. Arthritis Rheum. 2006;54:2271-9 pubmed
    ..The signal transduction leading to the SSc fibrotic phenotype appears to converge on DNA methylation and histone deacetylation at the FLI1 gene. ..
  5. Nozawa S, Ohno T, Banno Y, Dohjima T, Wakahara K, Fan D, et al. Inhibition of platelet-derived growth factor-induced cell growth signaling by a short interfering RNA for EWS-Fli1 via down-regulation of phospholipase D2 in Ewing sarcoma cells. J Biol Chem. 2005;280:27544-51 pubmed
    ..These results suggest that EWS-Fli1 may play a role in the regulation of tumor proliferation-signaling enzymes via PLD2 expression in Ewing sarcoma cells. ..
  6. Spyropoulos D, Pharr P, Lavenburg K, Jackers P, Papas T, Ogawa M, et al. Hemorrhage, impaired hematopoiesis, and lethality in mouse embryos carrying a targeted disruption of the Fli1 transcription factor. Mol Cell Biol. 2000;20:5643-52 pubmed
    ..Taken together, these results provide in vivo evidence for the role of Fli1 in the regulation of hematopoiesis and hemostasis. ..
  7. Knoop L, Baker S. The splicing factor U1C represses EWS/FLI-mediated transactivation. J Biol Chem. 2000;275:24865-71 pubmed
    ..Furthermore, they suggest that EWS and EWS/FLI may function both in transcriptional and post-transcriptional processes. ..
  8. Magnaghi Jaulin L, Masutani H, Robin P, Lipinski M, Harel Bellan A. SRE elements are binding sites for the fusion protein EWS-FLI-1. Nucleic Acids Res. 1996;24:1052-8 pubmed
    ..Taken together, our data indicate that there are intrinsic differences in the binding of EWS-FLI-1 and FLI-1 proteins to distinct ets sequences. ..
  9. Asano Y, Czuwara J, Trojanowska M. Transforming growth factor-beta regulates DNA binding activity of transcription factor Fli1 by p300/CREB-binding protein-associated factor-dependent acetylation. J Biol Chem. 2007;282:34672-83 pubmed
    ..Furthermore, these data strongly suggest that the TGF-beta-dependent acetylation of Fli1 may represent the principal mechanism responsible for the TGF-beta-induced dissociation of Fli1 from the collagen promoter. ..
  10. Bilke S, Schwentner R, Yang F, Kauer M, Jug G, Walker R, et al. Oncogenic ETS fusions deregulate E2F3 target genes in Ewing sarcoma and prostate cancer. Genome Res. 2013;23:1797-809 pubmed publisher
    ..Thus, EWSR1/FLI1 appears to promote oncogenesis by simultaneously promoting cell proliferation and perturbing differentiation. ..
  11. Prieur A, Tirode F, Cohen P, Delattre O. EWS/FLI-1 silencing and gene profiling of Ewing cells reveal downstream oncogenic pathways and a crucial role for repression of insulin-like growth factor binding protein 3. Mol Cell Biol. 2004;24:7275-83 pubmed
    ..Finally, IGFBP-3-induced Ewing cell apoptosis relies on both IGF-1-dependent and -independent pathways. These findings therefore identify the repression of IGFBP-3 as a key event in the development of Ewing's sarcoma. ..
  12. Le Deley M, Delattre O, Schaefer K, Burchill S, Koehler G, Hogendoorn P, et al. Impact of EWS-ETS fusion type on disease progression in Ewing's sarcoma/peripheral primitive neuroectodermal tumor: prospective results from the cooperative Euro-E.W.I.N.G. 99 trial. J Clin Oncol. 2010;28:1982-8 pubmed publisher
    ..10). CONCLUSION In contrast to retrospective studies, the prospective evaluation did not confirm a prognostic benefit for type 1 EWS-FLI1 fusions. ..
  13. Asano Y, Trojanowska M. Phosphorylation of Fli1 at threonine 312 by protein kinase C delta promotes its interaction with p300/CREB-binding protein-associated factor and subsequent acetylation in response to transforming growth factor beta. Mol Cell Biol. 2009;29:1882-94 pubmed publisher
    ..These data strongly suggest that the phosphorylation-acetylation cascade triggered by PKC delta represents the primary mechanism whereby TGF-beta regulates the transcriptional activity of Fli1 in the context of the collagen promoter. ..
  14. Nakerakanti S, Kapanadze B, Yamasaki M, Markiewicz M, Trojanowska M. Fli1 and Ets1 have distinct roles in connective tissue growth factor/CCN2 gene regulation and induction of the profibrotic gene program. J Biol Chem. 2006;281:25259-69 pubmed
    ..This study strongly supports a critical role of Fli1 and Ets1 in the pathological extracellular matrix regulation during fibrosis and cancer. ..
  15. van Doorninck J, Ji L, Schaub B, Shimada H, Wing M, Krailo M, et al. Current treatment protocols have eliminated the prognostic advantage of type 1 fusions in Ewing sarcoma: a report from the Children's Oncology Group. J Clin Oncol. 2010;28:1989-94 pubmed publisher
    ..CONCLUSION Current intensive treatment protocols for localized ESFT have erased the clinical disadvantage that was formerly observed in patients with non-type 1 EWS-FLI1 fusions. ..
  16. Delattre O, Zucman J, Plougastel B, Desmaze C, Melot T, Peter M, et al. Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours. Nature. 1992;359:162-5 pubmed
    ..Phylogenetically conserved restriction fragments in the vicinity of EWSR1 and EWSR2, the genomic regions where the breakpoints of chromosome 22 and chromosome 11 are, respectively, have allowed ..
  17. Zucman Rossi J, Legoix P, Victor J, Lopez B, Thomas G. Chromosome translocation based on illegitimate recombination in human tumors. Proc Natl Acad Sci U S A. 1998;95:11786-91 pubmed
    ..Taken together, these observations suggest that chromosome translocations in Ewing's tumors are mediated through a genuine illegitimate recombination mechanism. ..
  18. May W, Lessnick S, Braun B, Klemsz M, Lewis B, Lunsford L, et al. The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1. Mol Cell Biol. 1993;13:7393-8 pubmed
    ..EWS/FLI-1 could disrupt normal growth and differentiation either by more efficiently activating FLI-1 target genes or by inappropriately modulating genes normally not responsive to FLI-1. ..
  19. Li J, Chen Y, Zhang L, Xing L, Xu H, Wang Y, et al. Total saponins of panaxnotoginseng promotes lymphangiogenesis by activation VEGF-C expression of lymphatic endothelial cells. J Ethnopharmacol. 2016;193:293-302 pubmed publisher
  20. Schlums H, Jung M, Han H, Theorell J, Bigley V, Chiang S, et al. Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells. Blood. 2017;129:1927-1939 pubmed publisher
    ..In summary, adaptive NK cells can persist in patients with GATA2 mutation, even after NK-cell progenitors expire. Moreover, our data suggest that adaptive NK cells are more long-lived than canonical, immunoregulatory NK cells. ..
  21. Takahashi T, Asano Y, Nakamura K, Yamashita T, Saigusa R, Ichimura Y, et al. A potential contribution of antimicrobial peptide LL-37 to tissue fibrosis and vasculopathy in systemic sclerosis. Br J Dermatol. 2016;175:1195-1203 pubmed publisher
    ..LL-37 upregulation, induced by Fli1 deficiency at least in endothelial cells, potentially contributes to the development of skin sclerosis, interstitial lung disease and digital ulcers in SSc. ..
  22. Ichimiya Y, Wada Y, Kunishima S, Tsukamoto K, Kosaki R, Sago H, et al. 11q23 deletion syndrome (Jacobsen syndrome) with severe bleeding: a case report. J Med Case Rep. 2018;12:3 pubmed publisher
    ..We suggest that prenatal diagnosis and vigilant perinatal care including a cesarean section are warranted for patients with 11q23 deletion syndrome. ..
  23. Migueles R, Shaw L, Rodrigues N, May G, Henseleit K, Anderson K, et al. Transcriptional regulation of Hhex in hematopoiesis and hematopoietic stem cell ontogeny. Dev Biol. 2017;424:236-245 pubmed publisher
    ..The Hhex ECR thus appears to be a core node for the convergence of the transcription factor network that governs the emergence of HSCs. ..
  24. Yamashita T, Asano Y, Taniguchi T, Nakamura K, Saigusa R, Miura S, et al. Glycyrrhizin Ameliorates Fibrosis, Vasculopathy, and Inflammation in Animal Models of Systemic Sclerosis. J Invest Dermatol. 2017;137:631-640 pubmed publisher
  25. Morris E, Amria M, Kistner Griffin E, Svenson J, Kamen D, Gilkeson G, et al. A GA microsatellite in the Fli1 promoter modulates gene expression and is associated with systemic lupus erythematosus patients without nephritis. Arthritis Res Ther. 2010;12:R212 pubmed publisher
    ..Although no association between microsatellite length and lupus was observed, an association between a specific microsatellite length and patients without nephritis in the SLEIGH cohort was observed. ..
  26. Looney A, Han R, Stawski L, Marden G, Iwamoto M, Trojanowska M. Synergistic Role of Endothelial ERG and FLI1 in Mediating Pulmonary Vascular Homeostasis. Am J Respir Cell Mol Biol. 2017;57:121-131 pubmed publisher
    ..The goal of this study was to determine whether deficiencies of the ETS family member, Friend leukemia integration 1 transcription factor (FLI1), and its closest homolog, ETS-related gene (ERG), are associated with PAH...
  27. Patel M, Simon J, Iglesia M, Wu S, McFadden A, Lieb J, et al. Tumor-specific retargeting of an oncogenic transcription factor chimera results in dysregulation of chromatin and transcription. Genome Res. 2012;22:259-70 pubmed publisher
    ..Thus, the EWS-FLI chimera acquired chromatin-altering activity, leading to mistargeting, chromatin disruption, and ultimately, transcriptional dysregulation. ..
  28. Moore C, Parrish J, Jedlicka P. MiR-193b, downregulated in Ewing Sarcoma, targets the ErbB4 oncogene to inhibit anchorage-independent growth. PLoS ONE. 2017;12:e0178028 pubmed publisher
    ..Together, our studies show that the EWS/Fli1-repressed miR-193b is growth suppressive in Ewing Sarcoma, and identify ErbB4 as a target gene and candidate mediator of this growth suppression. ..
  29. Scheiber M, Watson P, Rumboldt T, Stanley C, Wilson R, Findlay V, et al. FLI1 expression is correlated with breast cancer cellular growth, migration, and invasion and altered gene expression. Neoplasia. 2014;16:801-13 pubmed publisher
    ..This study demonstrates a novel role for FLI1 in epithelial cells. In addition, these results reveal that FLI1 down-regulation in breast cancer may promote tumor progression. ..
  30. Owosho A, Ko E, Rosenberg H, Yom S, Antonescu C, Huryn J, et al. Primary Ewing Family of Tumors of the Jaw Has a Better Prognosis Compared to Tumors of Extragnathic Sites. J Oral Maxillofac Surg. 2016;74:973-81 pubmed publisher
    ..5 years. Patients with primary Ewing sarcoma of the jaw have a good prognosis and metastasis is an uncommon occurrence at initial presentation. ..
  31. Oh S, Shin S, Lightfoot S, Janknecht R. 14-3-3 proteins modulate the ETS transcription factor ETV1 in prostate cancer. Cancer Res. 2013;73:5110-9 pubmed publisher
    ..Finally, we showed that 14-3-3? and 14-3-3? were overexpressed in human prostate tumors. Taken together, our results showed that non-? 14-3-3 proteins are important modulators of ETV1 function that promote prostate tumorigenesis. ..
  32. Zöllner S, Selvanathan S, Graham G, Commins R, Hong S, Moseley E, et al. Inhibition of the oncogenic fusion protein EWS-FLI1 causes G2-M cell cycle arrest and enhanced vincristine sensitivity in Ewing's sarcoma. Sci Signal. 2017;10: pubmed publisher
    ..Thus, a combination of vincristine and YK-4-279 might be therapeutically effective in ES patients. ..
  33. Zhao H, Zhao Y, Li Z, Ouyang Q, Sun Y, Zhou D, et al. FLI1 and PKC co-activation promote highly efficient differentiation of human embryonic stem cells into endothelial-like cells. Cell Death Dis. 2018;9:131 pubmed publisher
    ..RNA-seq analysis verified that these cells closely resembled their in vivo counterparts. Our results showed that co-activation of FLI1 and PKC could induce differentiation of hESCs into iECs in a fast, efficient and economic manner. ..
  34. Mutz C, Schwentner R, Kauer M, Katschnig A, Kromp F, Aryee D, et al. EWS-FLI1 impairs aryl hydrocarbon receptor activation by blocking tryptophan breakdown via the kynurenine pathway. FEBS Lett. 2016;590:2063-75 pubmed publisher
    ..We demonstrate that EWS-FLI1 knockdown results in AHR nuclear translocation and activation. Our data suggest that EWS-FLI1 suppresses autocrine AHR signaling by inhibiting TDO2-catalyzed TRP breakdown. ..
  35. Chen J, Zhou W, Jia Q, Chen J, Zhang S, Yao W, et al. Efficient extravasation of tumor-repopulating cells depends on cell deformability. Sci Rep. 2016;6:19304 pubmed publisher
    ..Our findings suggest that tumor cell deformability is a key factor in controlling extravasation dynamics during metastasis. ..
  36. Beedie S, Peer C, Pisle S, Gardner E, Mahony C, Barnett S, et al. Anticancer Properties of a Novel Class of Tetrafluorinated Thalidomide Analogues. Mol Cancer Ther. 2015;14:2228-37 pubmed publisher
    ..This study establishes these novel thalidomide analogues as a promising immunomodulatory class with anticancer effects that warrant further development to characterize their mechanisms of action. ..
  37. Cuda J, Mirzamani N, Kantipudi R, Robbins J, Welsch M, Sundram U. Diagnostic utility of Fli-1 and D2-40 in distinguishing atypical fibroxanthoma from angiosarcoma. Am J Dermatopathol. 2013;35:316-8 pubmed publisher
    ..Thus, both D2-40 and Fli-1 seem to be useful in distinguishing between atypical fibroxanthomas and angiosarcomas. ..
  38. Stockley J, Morgan N, Bem D, Lowe G, Lordkipanidzé M, Dawood B, et al. Enrichment of FLI1 and RUNX1 mutations in families with excessive bleeding and platelet dense granule secretion defects. Blood. 2013;122:4090-3 pubmed publisher
    ..Our findings suggest that alterations in FLI1 and RUNX1 may be common in patients with platelet dense granule secretion defects and mild thrombocytopenia. ..
  39. Caropreso V, Darvishi E, Turbyville T, Ratnayake R, Grohar P, McMahon J, et al. Englerin A Inhibits EWS-FLI1 DNA Binding in Ewing Sarcoma Cells. J Biol Chem. 2016;291:10058-66 pubmed publisher
    ..This effect is mediated, at least in part, through a decrease in the levels of the calcium-dependent protein kinase PKC-βI after a transient up-regulation. ..
  40. Jacques C, Lamoureux F, Baud huin M, Rodriguez Calleja L, Quillard T, Amiaud J, et al. Targeting the epigenetic readers in Ewing sarcoma inhibits the oncogenic transcription factor EWS/Fli1. Oncotarget. 2016;7:24125-40 pubmed publisher
    ..Taken together, our data indicate that inhibiting the BET bromodomains interferes with EWS-FLi1 transcription and could be a promising strategy in the Ewing tumors context. ..
  41. Carpinelli M, Kruse E, Arhatari B, Debrincat M, Ogier J, Bories J, et al. Mice Haploinsufficient for Ets1 and Fli1 Display Middle Ear Abnormalities and Model Aspects of Jacobsen Syndrome. Am J Pathol. 2015;185:1867-76 pubmed publisher
    ..Our findings indicate that the short nose, otitis media, and hearing impairment in Jacobsen syndrome are likely because of hemizygosity for ETS1 and FLI1. ..
  42. Chai Y, Chipitsyna G, Cui J, Liao B, Liu S, Aysola K, et al. c-Fos oncogene regulator Elk-1 interacts with BRCA1 splice variants BRCA1a/1b and enhances BRCA1a/1b-mediated growth suppression in breast cancer cells. Oncogene. 2001;20:1357-67 pubmed
    ..All these results taken together suggest that one of the mechanisms by which BRCA1a/1b proteins function as growth/tumor suppressors is through inhibition of the expression of Elk-1 target genes like c-Fos. ..
  43. Mayoral Guisado C, Toro Zambrano W, López Macías M, Ruíz Guerrero A, Rubio Fernández A, Díaz Delgado M. [Pseudomyogenic hemangioendothelioma in the upper limb: A case report and literature review]. Rev Esp Patol. 2017;50:49-53 pubmed publisher
    ..We describe the clinical, histological, molecular and immunohistochemical features of pseudomyogenic hemangioendothelioma and review the pertinent literature. ..
  44. Tonon F, Zennaro C, Dapas B, Carraro M, Mariotti M, Grassi G. Rapid and cost-effective xenograft hepatocellular carcinoma model in Zebrafish for drug testing. Int J Pharm. 2016;515:583-591 pubmed publisher
    ..In conclusion, the possibility to test anti HCC/neo-angiogenesis drugs makes our JHH6 model useful to select therapeutic molecules for a highly vascularized tumor such as HCC. ..
  45. Asano Y. Epigenetic suppression of Fli1, a potential predisposing factor in the pathogenesis of systemic sclerosis. Int J Biochem Cell Biol. 2015;67:86-91 pubmed publisher
    ..b>Friend leukemia virus integration 1 (Fli1), a member of Ets transcription factor family, is epigenetically suppressed in the lesional ..
  46. Meng C, He Y, Peng C, Ding X, Guo L, Xiong L. Picrotoxane sesquiterpenoids from the stems of Dendrobium nobile and their absolute configurations and angiogenesis effect. Fitoterapia. 2017;121:206-211 pubmed publisher
    ..Compound 2 exhibited angiogenesis effect against sunitinib-induced damage on intersegmental blood vessels in Tg (flk1: EGFP) and Tg (fli1: nEGFP) transgenic zebrafish at concentrations of 3.13, 6.25, 12.50, and 25.00?M. ..
  47. Song W, Zhang T, Li W, Mu R, Zhang L, Li Y, et al. Overexpression of Fli-1 is associated with adverse prognosis of endometrial cancer. Cancer Invest. 2015;33:469-75 pubmed publisher
    This study aimed to investigate the expression of Friend leukemia virus integration 1 (Fli-1) and its correlation with the prognosis of endometrial cancer (EC)...
  48. Vo K, Jarocha D, Lyde R, Hayes V, Thom C, Sullivan S, et al. FLI1 level during megakaryopoiesis affects thrombopoiesis and platelet biology. Blood. 2017;129:3486-3494 pubmed publisher
    b>Friend leukemia virus integration 1 (FLI1), a critical transcription factor (TF) during megakaryocyte differentiation, is among genes hemizygously deleted in Jacobsen syndrome, resulting in a macrothrombocytopenia termed Paris-Trousseau ..
  49. Gierisch M, Pfistner F, Lopez Garcia L, Harder L, Schafer B, Niggli F. Proteasomal Degradation of the EWS-FLI1 Fusion Protein Is Regulated by a Single Lysine Residue. J Biol Chem. 2016;291:26922-26933 pubmed publisher
    ..Our study provides novel insights into EWS-FLI1 turnover, a critical pathway in Ewing sarcoma pathogenesis, and lays new ground to develop novel therapeutic strategies in Ewing sarcoma. ..
  50. Harlow M, Maloney N, ROLAND J, Guillén Navarro M, Easton M, Kitchen Goosen S, et al. Lurbinectedin Inactivates the Ewing Sarcoma Oncoprotein EWS-FLI1 by Redistributing It within the Nucleus. Cancer Res. 2016;76:6657-6668 pubmed publisher
    ..Our results illustrate the preclinical safety and efficacy of a disease-specific therapy targeting the central oncogenic driver in Ewing sarcoma. Cancer Res; 76(22); 6657-68. ©2016 AACR. ..
  51. Sakurai K, Fujiwara T, Hasegawa S, Okitsu Y, Fukuhara N, Onishi Y, et al. Inhibition of human primary megakaryocyte differentiation by anagrelide: a gene expression profiling analysis. Int J Hematol. 2016;104:190-9 pubmed publisher
    ..In conclusion, anagrelide suppresses megakaryocytic differentiation, partly through decreasing the expression of megakaryocytic transcription factors. ..
  52. Osgood C, Maloney N, Kidd C, Kitchen Goosen S, Segars L, Gebregiorgis M, et al. Identification of Mithramycin Analogues with Improved Targeting of the EWS-FLI1 Transcription Factor. Clin Cancer Res. 2016;22:4105-18 pubmed publisher
    ..Clin Cancer Res; 22(16); 4105-18. ©2016 AACR. ..
  53. Bonin G, Scamps C, Turc Carel C, Lipinski M. Chimeric EWS-FLI1 transcript in a Ewing cell line with a complex t(11;22;14) translocation. Cancer Res. 1993;53:3655-7 pubmed
    ..Direct sequencing was performed to demonstrate that the molecular rearrangement in this particular Ewing sample resulted in a fusion transcript similar to those observed in tumors with the prototypical translocation. ..
  54. McKinsey E, Parrish J, Irwin A, Niemeyer B, Kern H, Birks D, et al. A novel oncogenic mechanism in Ewing sarcoma involving IGF pathway targeting by EWS/Fli1-regulated microRNAs. Oncogene. 2011;30:4910-20 pubmed publisher
    ..This novel pathway may be amenable to innovative therapeutic targeting in Ewing sarcoma and other malignancies with activated IGF signaling. ..
  55. Tang S, Bilke S, Cao L, Murai J, Sousa F, Yamade M, et al. SLFN11 Is a Transcriptional Target of EWS-FLI1 and a Determinant of Drug Response in Ewing Sarcoma. Clin Cancer Res. 2015;21:4184-93 pubmed publisher
    ..Our results imply the emerging relevance of SLFN11 as an ETS transcription factor response gene and for therapeutic response to topoisomerase I inhibitors and temozolomide-PARP inhibitor combinations in ETS-activated cancers. ..
  56. Grohar P, Janeway K, Mase L, Schiffman J. Advances in the Treatment of Pediatric Bone Sarcomas. Am Soc Clin Oncol Educ Book. 2017;37:725-735 pubmed publisher
    ..In these patients through application of cost-effective evidence-based screening techniques the ultimate goal of cancer prevention is becoming a realization. ..
  57. Taniguchi T, Asano Y, Nakamura K, Yamashita T, Saigusa R, Ichimura Y, et al. Fli1 Deficiency Induces CXCL6 Expression in Dermal Fibroblasts and Endothelial Cells, Contributing to the Development of Fibrosis and Vasculopathy in Systemic Sclerosis. J Rheumatol. 2017;44:1198-1205 pubmed publisher
    ..We investigated the contribution of CXCL6 to SSc development by focusing on the association of friend leukemia virus integration 1 (Fli1) deficiency, a potential predisposing factor of SSc, with CXCL6 expression and clinical ..
  58. Wu L, Chen H, Zhu Y, Meng J, Li Y, Li M, et al. Flightless I homolog negatively regulates ChREBP activity in cancer cells. Int J Biochem Cell Biol. 2013;45:2688-97 pubmed publisher
    ..Our findings suggest that FLII is a component of the ChREBP transcriptional complex and negatively regulates ChREBP function in cancer cells. ..
  59. Grohar P, Glod J, Peer C, Sissung T, Arnaldez F, Long L, et al. A phase I/II trial and pharmacokinetic study of mithramycin in children and adults with refractory Ewing sarcoma and EWS-FLI1 fusion transcript. Cancer Chemother Pharmacol. 2017;80:645-652 pubmed publisher
    ..Evaluation of mithramycin in patients selected for decreased susceptibility to elevated transaminases may allow for improved drug exposure. ..
  60. Raslova H, Komura E, Le Couedic J, Larbret F, Debili N, Feunteun J, et al. FLI1 monoallelic expression combined with its hemizygous loss underlies Paris-Trousseau/Jacobsen thrombopenia. J Clin Invest. 2004;114:77-84 pubmed
  61. Park H, Turkalo T, Nelson K, Folmsbee S, Robb C, Roper B, et al. Ewing sarcoma EWS protein regulates midzone formation by recruiting Aurora B kinase to the midzone. Cell Cycle. 2014;13:2391-9 pubmed publisher
    ..Here, we propose that the impairment of EWS-dependent midzone formation via the recruitment of Aurora B is a potential mechanism of Ewing sarcoma development. ..
  62. Matrone G, Meng S, Gu Q, Lv J, Fang L, Chen K, et al. Lmo2 (LIM-Domain-Only 2) Modulates Sphk1 (Sphingosine Kinase) and Promotes Endothelial Cell Migration. Arterioscler Thromb Vasc Biol. 2017;37:1860-1868 pubmed publisher
    ..i>Lmo2 KD reduced Lmo2-Sphk1 gene interaction, impaired intersegmental vessels formation, and reduced cell migration. We identified for the first time Sphk1 as downstream effector of Lmo2. ..
  63. Tajima S, Takashi Y, Ito N, Fukumoto S, Fukuyama M. ERG and FLI1 are useful immunohistochemical markers in phosphaturic mesenchymal tumors. Med Mol Morphol. 2016;49:203-209 pubmed
    ..We concluded that ERG (or FLI1 if available) is useful marker for the diagnosis of PMT, and that PMTs may have an endothelial cell lineage. ..
  64. Lin S, Wu C, Chai C. Increased FLI-1 Expression is Associated With Poor Prognosis in Non-Small Cell Lung Cancers. Appl Immunohistochem Mol Morphol. 2016;24:556-61 pubmed publisher
    ..However, further studies are required to elucidate its function in tumorigenesis of NSCLC. ..
  65. Strickler A, Schaefer J, Slingluff C, Wick M. Immunolabeling for p16, WT1, and Fli-1 in the assignment of growth phase for cutaneous melanomas. Am J Dermatopathol. 2014;36:718-22 pubmed publisher
    ..At present, application of histological criteria remains the best method for assignment of growth phase in melanomas; however, p16 and possibly Fli-1 immunostains may serve as useful adjuncts in morphologically indeterminate cases. ..
  66. Minas T, Surdez D, Javaheri T, Tanaka M, Howarth M, Kang H, et al. Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model. Oncotarget. 2017;8:34141-34163 pubmed publisher
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    ..This interaction between EWSR1/FLI1 and EWSR1 in Ewing sarcoma may induce mitotic defects leading to genomic instability and subsequent malignant transformation. ..
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    ..These studies implicate the epigenetic downregulation of Fli1 and KLF5 as a central event triggering the pathogenic triad of SSc. ..
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    ..This is the first report presenting CD13/ANPEP and FLI1 as important mediators of resistance to BRAF inhibition with potential as drug targets in BRAFi refractory melanoma. ..
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    b>Friend leukemia virus integration 1 (FLI1), an Ets transcription factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events at the FLI1 locus, but the biologic impact of FLI1 expression on AML is unknown...
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