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Cited by 168Melanoma and MAPK PathwaysProtein Kinase Regulation and GTPase SignalingProtein Tyrosine Phosphatases

Emerging BRAF Mutations in Cancer Progression and Their Possible Effects on Transcriptional Networks

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Śmiech, Magdalena, Leszczyński, Paweł, Kono, Hidetoshi, Wardell, Christopher, Taniguchi, Hiroaki·2020·Genes
DOI 10.3390/genes11111342PMC PMC7697059
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Abstract

Gene mutations can induce cellular alteration and malignant transformation. Development of many types of cancer is associated with mutations in the B-raf proto-oncogene (BRAF) gene. The encoded protein is a component of the mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway, transmitting information from the outside to the cell nucleus. The main function of the MAPK/ERK pathway is to regulate cell growth, migration, and proliferation. The most common mutations in the BRAF gene encode the V600E mutant (class I), which causes continuous activation and signal transduction, regardless of external stimulus. Consequently, cell proliferation and invasion are enhanced in cancer patients with such mutations. The V600E mutation has been linked to melanoma, colorectal cancer, multiple myeloma, and other types of cancers. Importantly, emerging evidence has recently indicated that new types of mutations (classes II and III) also play a paramount role in the development of cancer. In this minireview, we discuss the influence of various BRAF mutations in cancer, including aberrant transcriptional gene regulation in the affected tissues.

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  • MAPK pathway-driven tumorigenesis, often induced by BRAFV600E, relies on epithelial dedifferentiation.

    “MAPK pathway-driven tumorigenesis, often induced by BRAFV600E, relies on epithelial dedifferentiation.”

    From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [24]

    Section 2 (page unavailable) identifies BRAF as an oncogenic driver in the MAPK/ERK pathway and says V600E increases cell proliferation. Section 5 suggests BRAF mutation-induced signaling can enhance epithelial-to-mesenchymal transition, but describes that process in relation to metastasis; it does not say MAPK-driven tumorigenesis relies on epithelial dedifferentiation. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Gene mutations of BRAF, especially BRAFV600E, and constitutively activated MAPK cascades drive multiple cancers, depriving differentiated features.

    “Gene mutations of BRAF, especially BRAFV600E, and constitutively activated MAPK cascades drive multiple types of cancers, depriving differentiated features through melanoma genesis and intestine/colon carcinogenesis24–27.”

    From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [24]

    Section 2 (Class I BRAF Mutations; page unavailable) describes BRAF V600E as constitutively active and BRAF as an oncogenic driver in cancers including melanoma and colorectal cancer. Section 6 reports increased proliferation in BRAF-mutated colorectal cancer cells. The cited passages do not establish that these cancers lose differentiated features, so that part of the claim is unsupported. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

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  1. [1]Kondoh K. Nishida E. Regulation of MAP Kinases by MAP Kinase Phosphatases Biochim. Biophys. Acta 2007 1773 1227 1237 10.1016/j.bbamcr.2006.12.002 17208316 · DOI
  2. [2]Robinson M.J. Cobb M.H. Mitogen-Activated Protein Kinase Pathways Curr. Opin. Cell Biol. 1997 9 180 186 10.1016/S0955-0674(97)80061-0 9069255 · DOI
  3. [3]Whitmarsh A.J. Regulation of Gene Transcription by Mitogen-Activated Protein Kinase Signaling Pathways Biochim. Biophys. Acta 2007 1773 1285 1298 10.1016/j.bbamcr.2006.11.011 17196680 · DOI
  4. [4]McCubrey J.A. Steelman L.S. Chappell W.H. Abrams S.L. Wong E.W. Chang F. Lehmann B. Terrian D.M. Milella M. Tafuri A. Roles of the Raf/MEK/ERK Pathway in Cell Growth, Malignant Transformation and Drug Resistance Biochim. Biophys. Acta 2007 1773 1263 1284 10.1016/j.bbamcr.2006.10.001 17126425 PMC2696318 · DOI
  5. [5]Murphy L.O. Blenis J. MAPK Signal Specificity: The Right Place at the Right Time Trends Biochem. Sci. 2006 31 268 275 10.1016/j.tibs.2006.03.009 16603362 · DOI · Paper page
  6. [6]Zhang W. Liu H.T. MAPK Signal Pathways in the Regulation of Cell Proliferation in Mammalian Cells Cell Res. 2002 12 9 18 10.1038/sj.cr.7290105 11942415 · DOI · Paper page
  7. [7]Garnett M.J. Marais R. Guilty as Charged: B-RAF is a Human Oncogene Cancer Cell 2004 6 313 319 10.1016/j.ccr.2004.09.022 15488754 · DOI
  8. [8]Zheng G. Tseng L.H. Chen G. Haley L. Illei P. Gocke C.D. Eshleman J.R. Lin M.T. Clinical Detection and Categorization of Uncommon and Concomitant Mutations Involving BRAF BMC Cancer 2015 15 779 10.1186/s12885-015-1811-y 26498038 PMC4619530 · DOI
  9. [9]Aramini J.M. Vorobiev S.M. Tuberty L.M. Janjua H. Campbell E.T. Seetharaman J. Su M. Huang Y.J. Acton T.B. Xiao R. The RAS-Binding Domain of Human BRAF Protein Serine/Threonine Kinase Exhibits Allosteric Conformational Changes upon Binding HRAS Structure 2015 23 1382 1393 10.1016/j.str.2015.06.003 26165597 PMC4963008 · DOI
  10. [10]Mandala M. Voit C. Targeting BRAF in Melanoma: Biological and Clinical Challenges Crit. Rev. Oncol. Hematol. 2013 87 239 255 10.1016/j.critrevonc.2013.01.003 23415641 · DOI
  11. [11]Roskoski R. Jr. RAF Protein-serine/threonine Kinases: Structure and Regulation Biochem. Biophys. Res. Commun. 2010 399 313 317 10.1016/j.bbrc.2010.07.092 20674547 · DOI
  12. [12]Wan P.T. Garnett M.J. Roe S.M. Lee S. Niculescu-Duvaz D. Good V.M. Jones C.M. Marshall C.J. Springer C.J. Barford D. Mechanism of Activation of the RAF-ERK Signaling Pathway by Oncogenic Mutations of B-RAF Cell 2004 116 855 867 10.1016/S0092-8674(04)00215-6 15035987 · DOI
  13. [13]Wenglowsky S. Ren L. Ahrendt K.A. Laird E.R. Aliagas I. Alicke B. Buckmelter A.J. Choo E.F. Dinkel V. Feng B. Pyrazolopyridine Inhibitors of B-Raf(V600E). Part 1: The Development of Selective, Orally Bioavailable, and Efficacious Inhibitors ACS Med. Chem. Lett. 2011 2 342 347 10.1021/ml200025q 24900315 PMC4017973 · DOI
  14. [14]Mason C.S. Springer C.J. Cooper R.G. Superti-Furga G. Marshall C.J. Marais R. Serine and Tyrosine Phosphorylations Cooperate in Raf-1, but Not B-Raf Activation EMBO J. 1999 18 2137 2148 10.1093/emboj/18.8.2137 10205168 PMC1171298 · DOI
  15. [15]Rahman M.A. Salajegheh A. Smith R.A. Lam A.K. B-Raf Mutation: A Key Player in Molecular Biology of Cancer Exp. Mol. Pathol. 2013 95 336 342 10.1016/j.yexmp.2013.10.005 24161954 · DOI
  16. [16]Haling J.R. Sudhamsu J. Yen I. Sideris S. Sandoval W. Phung W. Bravo B.J. Giannetti A.M. Peck A. Masselot A. Structure of the BRAF-MEK Complex Reveals a Kinase Activity Independent Role for BRAF in MAPK Signaling Cancer. Cell 2014 26 402 413 10.1016/j.ccr.2014.07.007 25155755 · DOI
  17. [17]Park E. Rawson S. Li K. Kim B.W. Ficarro S.B. Pino G.G. Sharif H. Marto J.A. Jeon H. Eck M.J. Architecture of Autoinhibited and Active BRAF-MEK1-14-3-3 Complexes Nature 2019 575 545 550 10.1038/s41586-019-1660-y 31581174 PMC7014971 · DOI
  18. [18]Cremolini C. Di Bartolomeo M. Amatu A. Antoniotti C. Moretto R. Berenato R. Perrone F. Tamborini E. Aprile G. Lonardi S. BRAF Codons 594 and 596 Mutations Identify a New Molecular Subtype of Metastatic Colorectal Cancer at Favorable Prognosis Ann. Oncol. 2015 26 2092 2097 10.1093/annonc/mdv290 26153495 · DOI
  19. [19]Wu X. Yan J. Dai J. Ma M. Tang H. Yu J. Xu T. Yu H. Si L. Chi Z. Mutations in BRAF Codons 594 and 596 Predict Good Prognosis in Melanoma Oncol. Lett. 2017 14 3601 3605 10.3892/ol.2017.6608 28927118 PMC5587919 · DOI
  20. [20]Boyle E.M. Ashby C. Tytarenko R. Deshpande S. Wang Y. Sawyer J. Tian E. Johnson S. Rutherford M.W. Wardell C.P. BRAF and DIS3 Mutations Associate with Adverse Outcome in a Long-Term Follow-Up of Patients with Multiple Myeloma Clin. Cancer Res. 2020 26 2422 2432 10.1158/1078-0432.CCR-19-1507 31988198 · DOI
  21. [21]Walker B.A. Mavrommatis K. Wardell C.P. Ashby T.C. Bauer M. Davies F.E. Rosenthal A. Wang H. Qu P. Hoering A. Identification of Novel Mutational Drivers Reveals Oncogene Dependencies in Multiple Myeloma Blood 2018 132 587 597 10.1182/blood-2018-03-840132 29884741 PMC6097138 · DOI · Paper page
  22. [22]Yao Z. Yaeger R. Rodrik-Outmezguine V.S. Tao A. Torres N.M. Chang M.T. Drosten M. Zhao H. Cecchi F. Hembrough T. Tumours with Class 3 BRAF Mutants are Sensitive to the Inhibition of Activated RAS Nature 2017 548 234 238 10.1038/nature23291 28783719 PMC5648058 · DOI · Paper page
  23. [23]Lin Q. Zhang H. Ding H. Qian J. Lizaso A. Lin J. Han-Zhang H. Xiang J. Li Y. Zhu H. The Association between BRAF Mutation Class and Clinical Features in BRAF-Mutant Chinese Non-Small Cell Lung Cancer Patients J. Transl. Med. 2019 17 298 10.1186/s12967-019-2036-7 31470866 PMC6716889 · DOI
  24. [25]Houben R. Becker J.C. Kappel A. Terheyden P. Brocker E.B. Goetz R. Rapp U.R. Constitutive Activation of the Ras-Raf Signaling Pathway in Metastatic Melanoma is Associated with Poor Prognosis J. Carcinog. 2004 3 6 10.1186/1477-3163-3-6 15046639 PMC420489 · DOI
  25. [26]Ikenoue T. Hikiba Y. Kanai F. Tanaka Y. Imamura J. Imamura T. Ohta M. Ijichi H. Tateishi K. Kawakami T. Functional Analysis of Mutations within the Kinase Activation Segment of B-Raf in Human Colorectal Tumors Cancer Res. 2003 63 8132 8137 14678966
  26. [27]Lin K.L. Wang O.C. Zhang X.H. Dai X.X. Hu X.Q. Qu J.M. The BRAF Mutation is Predictive of Aggressive Clinicopathological Characteristics in Papillary Thyroid Microcarcinoma Ann. Surg. Oncol. 2010 17 3294 3300 10.1245/s10434-010-1129-6 20953721 · DOI
  27. [28]Naoki K. Chen T.H. Richards W.G. Sugarbaker D.J. Meyerson M. Missense Mutations of the BRAF Gene in Human Lung Adenocarcinoma Cancer Res. 2002 62 7001 7003 12460919
  28. [29]Sadlecki P. Walentowicz P. Bodnar M. Marszalek A. Grabiec M. Walentowicz-Sadlecka M. Determination of BRAF V600E (VE1) Protein Expression and BRAF Gene Mutation Status in Codon 600 in Borderline and Low-Grade Ovarian Cancers Tumour Biol. 2017 39 10.1177/1010428317706230 28488545 · DOI
  29. [30]Andrulis M. Lehners N. Capper D. Penzel R. Heining C. Huellein J. Zenz T. von Deimling A. Schirmacher P. Ho A.D. Targeting the BRAF V600E Mutation in Multiple Myeloma Cancer Discov. 2013 3 862 869 10.1158/2159-8290.CD-13-0014 23612012 · DOI
  30. [31]Wimmer R. Baccarini M. Partner Exchange: Protein-Protein Interactions in the Raf Pathway Trends Biochem. Sci. 2010 35 660 668 10.1016/j.tibs.2010.06.001 20621483 · DOI
  31. [32]Cantwell-Dorris E.R. O’Leary J.J. Sheils O.M. BRAFV600E: Implications for Carcinogenesis and Molecular Therapy Mol. Cancer Ther. 2011 10 385 394 10.1158/1535-7163.MCT-10-0799 21388974 · DOI
  32. [33]Lavoie H. Therrien M. Regulation of RAF Protein Kinases in ERK Signalling Nat. Rev. Mol. Cell Biol. 2015 16 281 298 10.1038/nrm3979 25907612 · DOI
  33. [34]Schirripa M. Biason P. Lonardi S. Pella N. Pino M.S. Urbano F. Antoniotti C. Cremolini C. Corallo S. Pietrantonio F. Class 1, 2, and 3 BRAF-Mutated Metastatic Colorectal Cancer: A Detailed Clinical, Pathologic, and Molecular Characterization Clin. Cancer Res. 2019 25 3954 3961 10.1158/1078-0432.CCR-19-0311 30967421 · DOI
  34. [35]Moretti S. De Falco V. Tamburrino A. Barbi F. Tavano M. Avenia N. Santeusanio F. Santoro M. Macchiarulo A. Puxeddu E. Insights into the Molecular Function of the Inactivating Mutations of B-Raf Involving the DFG Motif Biochim. Biophys. Acta 2009 1793 1634 1645 10.1016/j.bbamcr.2009.09.001 19735675 · DOI
  35. [36]Hari S.B. Merritt E.A. Maly D.J. Sequence Determinants of a Specific Inactive Protein Kinase Conformation Chem. Biol. 2013 20 806 815 10.1016/j.chembiol.2013.05.005 23790491 PMC3742363 · DOI
  36. [37]Vijayan R.S. He P. Modi V. Duong-Ly K.C. Ma H. Peterson J.R. Dunbrack R.L. Jr. Levy R.M. Conformational Analysis of the DFG-Out Kinase Motif and Biochemical Profiling of Structurally Validated Type II Inhibitors J. Med. Chem. 2015 58 466 479 10.1021/jm501603h 25478866 PMC4326797 · DOI
  37. [38]Johnson L.N. Lowe E.D. Noble M.E. Owen D.J. The Eleventh Datta Lecture. the Structural Basis for Substrate Recognition and Control by Protein Kinases FEBS Lett. 1998 430 1 11 10.1016/S0014-5793(98)00606-1 9678585 · DOI
  38. [39]Garnett M.J. Rana S. Paterson H. Barford D. Marais R. Wild-Type and Mutant B-RAF Activate C-RAF through Distinct Mechanisms Involving Heterodimerization Mol. Cell 2005 20 963 969 10.1016/j.molcel.2005.10.022 16364920 · DOI
  39. [40]Heidorn S.J. Milagre C. Whittaker S. Nourry A. Niculescu-Duvas I. Dhomen N. Hussain J. Reis-Filho J.S. Springer C.J. Pritchard C. Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF Cell 2010 140 209 221 10.1016/j.cell.2009.12.040 20141835 PMC2872605 · DOI
  40. [41]Scholl F.A. Dumesic P.A. Khavari P.A. Effects of Active MEK1 Expression in Vivo Cancer Lett. 2005 230 1 5 10.1016/j.canlet.2004.12.013 16253755 · DOI
  41. [42]Maik-Rachline G. Hacohen-Lev-Ran A. Seger R. Nuclear ERK: Mechanism of Translocation, Substrates, and Role in Cancer Int. J. Mol. Sci. 2019 20 1194 10.3390/ijms20051194 PMC6429060 30857244 · DOI
  42. [43]Pulverer B.J. Fisher C. Vousden K. Littlewood T. Evan G. Woodgett J.R. Site-Specific Modulation of c-Myc Cotransformation by Residues Phosphorylated in Vivo Oncogene 1994 9 59 70 8302604
  43. [44]Sears R. Nuckolls F. Haura E. Taya Y. Tamai K. Nevins J.R. Multiple Ras-Dependent Phosphorylation Pathways Regulate Myc Protein Stability Genes Dev. 2000 14 2501 2514 10.1101/gad.836800 11018017 PMC316970 · DOI
  44. [45]Liu H. Ai J. Shen A. Chen Y. Wang X. Peng X. Chen H. Shen Y. Huang M. Ding J. C-Myc Alteration Determines the Therapeutic Response to FGFR Inhibitors Clin. Cancer Res. 2017 23 974 984 10.1158/1078-0432.CCR-15-2448 27401245 · DOI
  45. [46]Lan H.Y. Diverse Roles of TGF-beta/Smads in Renal Fibrosis and Inflammation Int. J. Biol. Sci. 2011 7 1056 1067 10.7150/ijbs.7.1056 21927575 PMC3174390 · DOI
  46. [47]Brabletz T. Kalluri R. Nieto M.A. Weinberg R.A. EMT in Cancer Nat. Rev. Cancer 2018 18 128 134 10.1038/nrc.2017.118 29326430 · DOI · Paper page
  47. [48]Dongre A. Weinberg R.A. New Insights into the Mechanisms of Epithelial-Mesenchymal Transition and Implications for Cancer Nat. Rev. Mol. Cell Biol. 2019 20 69 84 10.1038/s41580-018-0080-4 30459476 · DOI · Paper page
  48. [49]Guo Y. Cui W. Pei Y. Xu D. Platelets Promote Invasion and Induce Epithelial to Mesenchymal Transition in Ovarian Cancer Cells by TGF-Beta Signaling Pathway Gynecol. Oncol. 2019 153 639 650 10.1016/j.ygyno.2019.02.026 30928020 · DOI
  49. [50]Wang X.L. Huang C. Difference of TGF-beta/Smads Signaling Pathway in Epithelial-Mesenchymal Transition of Normal Colonic Epithelial Cells Induced by Tumor-Associated Fibroblasts and Colon Cancer Cells Mol. Biol. Rep. 2019 46 2749 2759 10.1007/s11033-019-04719-5 30835040 · DOI
  50. [51]Zipper L.M. Mulcahy R.T. Erk Activation is Required for Nrf2 Nuclear Localization during Pyrrolidine Dithiocarbamate Induction of Glutamate Cysteine Ligase Modulatory Gene Expression in HepG2 Cells Toxicol. Sci. 2003 73 124 134 10.1093/toxsci/kfg083 12657749 · DOI
  51. [52]Cho S.J. Ryu J.H. Surh Y.J. Ajoene, a Major Organosulfide found in Crushed Garlic, Induces NAD(P)H:Quinone Oxidoreductase Expression through Nuclear Factor E2-Related Factor-2 Activation in Human Breast Epithelial Cells J. Cancer Prev. 2019 24 112 122 10.15430/JCP.2019.24.2.112 31360690 PMC6619855 · DOI
  52. [53]Jang H.J. Hong E.M. Kim M. Kim J.H. Jang J. Park S.W. Byun H.W. Koh D.H. Choi M.H. Kae S.H. Simvastatin Induces Heme Oxygenase-1 Via NF-E2-Related Factor 2 (Nrf2) Activation through ERK and PI3K/Akt Pathway in Colon Cancer Oncotarget 2016 7 46219 46229 10.18632/oncotarget.10078 27323826 PMC5216792 · DOI
  53. [54]Bai X. Gou X. Cai P. Xu C. Cao L. Zhao Z. Huang M. Jin J. Sesamin Enhances Nrf2-Mediated Protective Defense Against Oxidative Stress and Inflammation in Colitis Via AKT and ERK Activation Oxidative Med. Cell. Longev. 2019 2019 2432416 10.1155/2019/2432416 PMC6732632 31534619 · DOI
  54. [55]Bucolo C. Drago F. Maisto R. Romano G.L. D’Agata V. Maugeri G. Giunta S. Curcumin Prevents High Glucose Damage in Retinal Pigment Epithelial Cells through ERK1/2-Mediated Activation of the Nrf2/HO-1 Pathway J. Cell. Physiol. 2019 234 17295 17304 10.1002/jcp.28347 30770549 · DOI
  55. [56]DeNicola G.M. Karreth F.A. Humpton T.J. Gopinathan A. Wei C. Frese K. Mangal D. Yu K.H. Yeo C.J. Calhoun E.S. Oncogene-Induced Nrf2 Transcription Promotes ROS Detoxification and Tumorigenesis Nature 2011 475 106 109 10.1038/nature10189 21734707 PMC3404470 · DOI · Paper page
  56. [57]Zimta A.A. Cenariu D. Irimie A. Magdo L. Nabavi S.M. Atanasov A.G. Berindan-Neagoe I. The Role of Nrf2 Activity in Cancer Development and Progression Cancers 2019 11 1755 10.3390/cancers11111755 PMC6896028 31717324 · DOI
  57. [58]Huilgol D. Venkataramani P. Nandi S. Bhattacharjee S. Transcription Factors that Govern Development and Disease: An Achilles Heel in Cancer Genes 2019 10 794 10.3390/genes10100794 PMC6826716 31614829 · DOI
  58. [59]Tremblay M. Sanchez-Ferras O. Bouchard M. GATA Transcription Factors in Development and Disease Development 2018 145 10.1242/dev.164384 30348673 · DOI
  59. [60]Bonner A.E. Lemon W.J. You M. Gene Expression Signatures Identify Novel Regulatory Pathways during Murine Lung Development: Implications for Lung Tumorigenesis J. Med. Genet. 2003 40 408 417 10.1136/jmg.40.6.408 12807961 PMC1735509 · DOI
  60. [61]Ma R. Li X. Liu H. Jiang R. Yang M. Zhang M. Wang Y. Zhao Y. Li H. GATA6-Upregulating Autophagy Promotes TKI Resistance in Nonsmall Cell Lung Cancer Cancer Biol. Ther. 2019 20 1206 1212 10.1080/15384047.2019.1599665 31092103 PMC6741565 · DOI
  61. [62]Sun Z. Yan B. Multiple Roles and Regulatory Mechanisms of the Transcription Factor GATA6 in Human Cancers Clin. Genet. 2020 97 64 72 10.1111/cge.13630 31437305 · DOI
  62. [63]Halmos B. Basseres D.S. Monti S. D’Alo F. Dayaram T. Ferenczi K. Wouters B.J. Huettner C.S. Golub T.R. Tenen D.G. A Transcriptional Profiling Study of CCAAT/enhancer Binding Protein Targets Identifies Hepatocyte Nuclear Factor 3 Beta as a Novel Tumor Suppressor in Lung Cancer Cancer Res. 2004 64 4137 4147 10.1158/0008-5472.CAN-03-4052 15205324 · DOI
  63. [64]Adachi Y. Shibai Y. Mitsushita J. Shang W.H. Hirose K. Kamata T. Oncogenic Ras Upregulates NADPH Oxidase 1 Gene Expression through MEK-ERK-Dependent Phosphorylation of GATA-6 Oncogene 2008 27 4921 4932 10.1038/onc.2008.133 18454176 · DOI
  64. [65]Sekiya S. Suzuki A. Direct Conversion of Mouse Fibroblasts to Hepatocyte-Like Cells by Defined Factors Nature 2011 475 390 393 10.1038/nature10263 21716291 · DOI · Paper page
  65. [66]Huang P. He Z. Ji S. Sun H. Xiang D. Liu C. Hu Y. Wang X. Hui L. Induction of Functional Hepatocyte-Like Cells from Mouse Fibroblasts by Defined Factors Nature 2011 475 386 389 10.1038/nature10116 21562492 · DOI · Paper page
  66. [67]Enane F.O. Shuen W.H. Gu X. Quteba E. Przychodzen B. Makishima H. Bodo J. Ng J. Chee C.L. Ba R. GATA4 Loss of Function in Liver Cancer Impedes Precursor to Hepatocyte Transition J. Clin. Investig. 2017 127 3527 3542 10.1172/JCI93488 28758902 PMC5669578 · DOI
  67. [68]Fan T.T. Hu P.F. Wang J. Wei J. Zhang Q. Ning B.F. Yin C. Zhang X. Xie W.F. Chen Y.X. Regression Effect of Hepatocyte Nuclear Factor 4alpha on Liver Cirrhosis in Rats J. Dig. Dis. 2013 14 318 327 10.1111/1751-2980.12042 23374293 · DOI
  68. [69]Ning B.F. Ding J. Yin C. Zhong W. Wu K. Zeng X. Yang W. Chen Y.X. Zhang J.P. Zhang X. Hepatocyte Nuclear Factor 4 Alpha Suppresses the Development of Hepatocellular Carcinoma Cancer Res. 2010 70 7640 7651 10.1158/0008-5472.CAN-10-0824 20876809 · DOI
  69. [70]Smallridge R.C. Chindris A.M. Asmann Y.W. Casler J.D. Serie D.J. Reddi H.V. Cradic K.W. Rivera M. Grebe S.K. Necela B.M. RNA Sequencing Identifies Multiple Fusion Transcripts, Differentially Expressed Genes, and Reduced Expression of Immune Function Genes in BRAF (V600E) Mutant Vs BRAF Wild-Type Papillary Thyroid Carcinoma J. Clin. Endocrinol. Metab. 2014 99 E338 E347 10.1210/jc.2013-2792 24297791 PMC3913813 · DOI
  70. [71]Qu Y. Yang Q. Liu J. Shi B. Ji M. Li G. Hou P. C-Myc is Required for BRAF(V600E)-Induced Epigenetic Silencing by H3K27me3 in Tumorigenesis Theranostics 2017 7 2092 2107 10.7150/thno.19884 28656062 PMC5485424 · DOI
  71. [72]Angell T.E. Lechner M.G. Jang J.K. Correa A.J. LoPresti J.S. Epstein A.L. BRAF V600E in Papillary Thyroid Carcinoma is Associated with Increased Programmed Death Ligand 1 Expression and Suppressive Immune Cell Infiltration Thyroid 2014 24 1385 1393 10.1089/thy.2014.0134 24955518 PMC4148060 · DOI
  72. [73]Flockhart R.J. Webster D.E. Qu K. Mascarenhas N. Kovalski J. Kretz M. Khavari P.A. BRAFV600E Remodels the Melanocyte Transcriptome and Induces BANCR to Regulate Melanoma Cell Migration Genome Res. 2012 22 1006 1014 10.1101/gr.140061.112 22581800 PMC3371703 · DOI · Paper page
  73. [74]Kochi M. Hinoi T. Niitsu H. Miguchi M. Saito Y. Sada H. Sentani K. Sakamoto N. Oue N. Tashiro H. Oncogenic Mutation in RAS-RAF Axis Leads to Increased Expression of GREB1, Resulting in Tumor Proliferation in Colorectal Cancer Cancer Sci. 2020 111 3540 3549 10.1111/cas.14558 32629543 PMC7541019 · DOI
  74. [75]Cao Y.M. Gu J. Zhang Y.S. Wei W.J. Qu N. Wen D. Liao T. Shi R.L. Zhang L. Ji Q.H. Aberrant Hypermethylation of the HOXD10 Gene in Papillary Thyroid Cancer with BRAFV600E Mutation Oncol. Rep. 2018 39 338 348 10.3892/or.2017.6058 29115628 · DOI
  75. [76]Rusinek D. Swierniak M. Chmielik E. Kowal M. Kowalska M. Cyplinska R. Czarniecka A. Piglowski W. Korfanty J. Chekan M. BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma PLoS ONE 2015 10 e0143688 10.1371/journal.pone.0143688 26625260 PMC4666467 · DOI
  76. [77]Barros-Filho M.C. de Mello J.B.H. Marchi F.A. Pinto C.A.L. da Silva I.C. Damasceno P.K.F. Soares M.B.P. Kowalski L.P. Rogatto S.R. GADD45B Transcript is a Prognostic Marker in Papillary Thyroid Carcinoma Patients Treated with Total Thyroidectomy and Radioiodine Therapy Front. Endocrinol. 2020 11 269 10.3389/fendo.2020.00269 PMC7203742 32425887 · DOI
  77. [78]Rusinek D. Pfeifer A. Cieslicka M. Kowalska M. Pawlaczek A. Krajewska J. Szpak-Ulczok S. Tyszkiewicz T. Halczok M. Czarniecka A. TERT Promoter Mutations and their Impact on Gene Expression Profile in Papillary Thyroid Carcinoma Cancers 2020 12 1597 10.3390/cancers12061597 PMC7352936 32560331 · DOI
  78. [79]Wongchenko M.J. McArthur G.A. Dreno B. Larkin J. Ascierto P.A. Sosman J. Andries L. Kockx M. Hurst S.D. Caro I. Gene Expression Profiling in BRAF-Mutated Melanoma Reveals Patient Subgroups with Poor Outcomes to Vemurafenib that may be Overcome by Cobimetinib Plus Vemurafenib Clin. Cancer Res. 2017 23 5238 5245 10.1158/1078-0432.CCR-17-0172 28536307 · DOI
  79. [80]Patel H. Yacoub N. Mishra R. White A. Long Y. Alanazi S. Garrett J.T. Current Advances in the Treatment of BRAF-Mutant Melanoma Cancers 2020 12 482 10.3390/cancers12020482 PMC7072236 32092958 · DOI

Cited by

Sorted by citations

Authors
Śmiech, M., Leszczyński, P., Kono, H., Wardell, C., & Taniguchi, H.
Affiliations
  • Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences (PL)
  • National Institutes for Quantum Science and Technology (JP)
  • University of Arkansas for Medical Sciences (US)
Corresponding author
Taniguchi, Hiroaki
ORCID
Venue
Genes
Publisher
MDPI AG
Published
2020-11-12
Volume
11
Issue
11
Pages
1342
ISSN
2073-4425 (ISSN-L)
DOI
10.3390/genes11111342
PMC
PMC7697059
OpenAlex
W3103114756
Cited by
168
References
1
Citations by year
2026: 23 · 2025: 37 · 2024: 59 · 2023: 31 · 2022: 13 · 2021: 5
FWCI
1.20
Type
journal article
Language
en
Open access
Licence
Locations
  • Genes (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • QST-Repository (National Institutes for Quantum and Radiological Science and Technology) (submittedVersion, cc-by-nc-nd)
Funders
Narodowym Centrum Nauki (2017/25/N/NZ5/01885)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords
BRAF mutation, BRAF V600E mutation, MAPK/ERK pathway, tumor progression, melanoma, colorectal cancer, multiple myeloma, cell proliferation, cell invasion
MeSH terms
Proto-Oncogene Mas, Humans, Mutation, Neoplasms, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins B-raf, Gene Regulatory Networks

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