دورية أكاديمية
أعرض في EDS

Combined Inhibition of HDAC and EGFR Reduces Viability and Proliferation and Enhances STAT3 mRNA Expression in Glioblastoma Cells.

التفاصيل البيبلوغرافية
العنوان: Combined Inhibition of HDAC and EGFR Reduces Viability and Proliferation and Enhances STAT3 mRNA Expression in Glioblastoma Cells.
المؤلفون: Buendia Duque M; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil., Pinheiro KV; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil., Thomaz A; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil., da Silva CA; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil., Freire NH; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil., Brunetto AT; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Children's Cancer Institute, Porto Alegre, RS, 90620-110, Brazil., Schwartsmann G; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Internal Medicine, Faculty of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil., Jaeger M; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil.; Children's Cancer Institute, Porto Alegre, RS, 90620-110, Brazil., de Farias CB; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.; Children's Cancer Institute, Porto Alegre, RS, 90620-110, Brazil., Roesler R; Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil. rafaelroesler@hcpa.edu.br.; Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil. rafaelroesler@hcpa.edu.br.
المصدر: Journal of molecular neuroscience : MN [J Mol Neurosci] 2019 May; Vol. 68 (1), pp. 49-57. Date of Electronic Publication: 2019 Mar 18.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Humana Press Country of Publication: United States NLM ID: 9002991 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-1166 (Electronic) Linking ISSN: 08958696 NLM ISO Abbreviation: J Mol Neurosci Subsets: MEDLINE
أسماء مطبوعة: Publication: Totowa, NJ : Humana Press
Original Publication: Boston : Birkhäuser [i.e. Cambridge, MA : Birkhäuser Boston, c1989-
مواضيع طبية MeSH: Antineoplastic Agents/*pharmacology , Brain Neoplasms/*metabolism , ErbB Receptors/*antagonists & inhibitors , Glioblastoma/*metabolism , Histone Deacetylase Inhibitors/*pharmacology , STAT3 Transcription Factor/*genetics, Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Humans ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; STAT3 Transcription Factor/metabolism
مستخلص: Changes in expression of histone deacetylases (HDACs), which epigenetically regulate chromatin structure, and mutations and amplifications of the EGFR gene, which codes for the epidermal growth factor receptor (EGFR), have been reported in glioblastoma (GBM), the most common and malignant type of brain tumor. There are likely interplays between HDACs and EGFR in promoting GBM progression, and HDAC inhibition can cooperate with EGFR blockade in reducing the growth of lung cancer cells. Here, we found that either HDAC or EGFR inhibitors dose-dependently reduced the viability of U87 and A-172 human GBM cells. In U87 cells, the combined inhibition of HDACs and EGFR was more effective than inhibiting either target alone in reducing viability and long-term proliferation. In addition, HDAC or EGFR inhibition, alone or combined, led to G0/G1 cell cycle arrest. The EGFR inhibitor alone or combined with HDAC inhibition increased mRNA expression of the signal transducer and activator of transcription 3 (STAT3), which can act either as an oncogene or a tumor suppressor in GBM. These data provide early evidence that combining HDAC and EGFR inhibition may be an effective strategy to reduce GBM growth, through a mechanism possibly involving STAT3.
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معلومات مُعتمدة: 303276/2013-4 National Council for Scientific and Technological Development (CNPq); 409287/2016-4 National Council for Scientific and Technological Development (CNPq)
فهرسة مساهمة: Keywords: Brain tumor; Chromatin; Epidermal growth factor receptor; Glioblastoma; Growth factor receptor; Histone deacetylase
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Histone Deacetylase Inhibitors)
0 (RNA, Messenger)
0 (STAT3 Transcription Factor)
0 (STAT3 protein, human)
EC 2.7.10.1 (ErbB Receptors)
تواريخ الأحداث: Date Created: 20190320 Date Completed: 20190529 Latest Revision: 20210109
رمز التحديث: 20221213
DOI: 10.1007/s12031-019-01280-5
PMID: 30887411
قاعدة البيانات: MEDLINE
الوصف
تدمد:1559-1166
DOI:10.1007/s12031-019-01280-5