دورية أكاديمية
أعرض في EDS

Suppression of microRNA-9 by mutant EGFR signaling upregulates FOXP1 to enhance glioblastoma tumorigenicity.

التفاصيل البيبلوغرافية
العنوان: Suppression of microRNA-9 by mutant EGFR signaling upregulates FOXP1 to enhance glioblastoma tumorigenicity.
المؤلفون: Gomez GG; Authors' Affiliations: Ludwig Institute for Cancer Research, University of California San Diego, La Jolla, California; Department of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio; Department of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Neurology, Washington University School of Medicine, St. Louis, Missouri; and Department of Neurosurgery, Memorial Sloan-Kettering Cancer Center, New York, New York., Volinia S, Croce CM, Zanca C, Li M, Emnett R, Gutmann DH, Brennan CW, Furnari FB, Cavenee WK
المصدر: Cancer research [Cancer Res] 2014 Mar 01; Vol. 74 (5), pp. 1429-39. Date of Electronic Publication: 2014 Jan 16.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1538-7445 (Electronic) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, Md. : American Association for Cancer Research
Original Publication: Chicago [etc.]
مواضيع طبية MeSH: Carcinogenesis/*genetics , ErbB Receptors/*genetics , Forkhead Transcription Factors/*genetics , Glioblastoma/*genetics , Glioblastoma/*pathology , MicroRNAs/*genetics , Signal Transduction/*genetics, Animals ; Carcinogenesis/pathology ; Humans ; Mice ; Mutation/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Tumor Cells, Cultured ; Up-Regulation ; ras Proteins/genetics
مستخلص: The EGF receptor (EGFR) is amplified and mutated in glioblastoma, in which its common mutation (ΔEGFR, also called EGFRvIII) has a variety of activities that promote growth and inhibit death, thereby conferring a strong tumor-enhancing effect. This range of activities suggested to us that ΔEGFR might exert its influence through pleiotropic effectors, and we hypothesized that microRNAs might serve such a function. Here, we report that ΔEGFR specifically suppresses one such microRNA, namely miR-9, through the Ras/PI3K/AKT axis that it is known to activate. Correspondingly, expression of miR-9 antagonizes the tumor growth advantage conferred by ΔEGFR. Silencing of FOXP1, a miR-9 target, inhibits ΔEGFR-dependent tumor growth and, conversely, de-repression of FOXP1, as a consequence of miR-9 inhibition, increases tumorigenicity. FOXP1 was sufficient to increase tumor growth in the absence of oncogenic ΔEGFR signaling. The significance of these findings is underscored by our finding that high FOXP1 expression predicts poor survival in a cohort of 131 patients with glioblastoma. Collectively, these data suggest a novel regulatory mechanism by which ΔEGFR suppression of miR-9 upregulates FOXP1 to increase tumorigenicity.
(©2014 AACR)
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معلومات مُعتمدة: R01-NS080939 United States NS NINDS NIH HHS; P01 CA095616 United States CA NCI NIH HHS; P30 CA023100 United States CA NCI NIH HHS; P30 CA016058 United States CA NCI NIH HHS; R01 NS080939 United States NS NINDS NIH HHS; P01-CA95616 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Forkhead Transcription Factors)
0 (MicroRNAs)
EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
EC 2.7.10.1 (ErbB Receptors)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 3.6.5.2 (ras Proteins)
تواريخ الأحداث: Date Created: 20140118 Date Completed: 20140603 Latest Revision: 20220316
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3947420
DOI: 10.1158/0008-5472.CAN-13-2117
PMID: 24436148
قاعدة البيانات: MEDLINE
الوصف
تدمد:1538-7445
DOI:10.1158/0008-5472.CAN-13-2117