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      GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways

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          Abstract

          The general control of nucleotide synthesis 5 (GCN5), which is one kind of lysine acetyltransferases, regulates a number of cellular processes, such as cell proliferation, differentiation, cell cycle and DNA damage repair. However, its biological role in human glioma development remains elusive. In the present study, we firstly reported that GCN5 was frequently overexpressed in human glioma tissues and GCN5 was positively correlated with proliferation of cell nuclear antigen PCNA and matrix metallopeptidase MMP9. Meanwhile, down-regulation of GCN5 by siRNA interfering inhibited glioma cell proliferation and invasion. In addition, GCN5 knockdown reduced expression of p-STAT3, p-AKT, PCNA and MMP9 and increased the expression of p21 in glioma cells. In conclusion, GCN5 exhibited critical roles in glioma development by regulating cell proliferation and invasion, which suggested that GCN5 might be a potential molecular target for glioma treatment.

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          The role of histone deacetylases (HDACs) in human cancer.

          Santiago Ropero, Manel Esteller (2007)
          The balance of histone acetylation and deacetylation is an epigenetic layer with a critical role in the regulation of gene expression. Histone acetylation induced by histone acetyl transferases (HATs) is associated with gene transcription, while histone hypoacetylation induced by histone deacetylase (HDAC) activity is associated with gene silencing. Altered expression and mutations of genes that encode HDACs have been linked to tumor development since they both induce the aberrant transcription of key genes regulating important cellular functions such as cell proliferation, cell-cycle regulation and apoptosis. Thus, HDACs are among the most promising therapeutic targets for cancer treatment, and they have inspired researchers to study and develop HDAC inhibitors.
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            Distinct roles of GCN5/PCAF-mediated H3K9ac and CBP/p300-mediated H3K18/27ac in nuclear receptor transactivation.

            Qihuang Jin, Li-Rong Yu, Lifeng Wang … (2011)
            Histone acetyltransferases (HATs) GCN5 and PCAF (GCN5/PCAF) and CBP and p300 (CBP/p300) are transcription co-activators. However, how these two distinct families of HATs regulate gene activation remains unclear. Here, we show deletion of GCN5/PCAF in cells specifically and dramatically reduces acetylation on histone H3K9 (H3K9ac) while deletion of CBP/p300 specifically and dramatically reduces acetylations on H3K18 and H3K27 (H3K18/27ac). A ligand for nuclear receptor (NR) PPARδ induces sequential enrichment of H3K18/27ac, RNA polymerase II (Pol II) and H3K9ac on PPARδ target gene Angptl4 promoter, which correlates with a robust Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9ac, but not H3K18/27ac, on the Angptl4 promoter. Finally, we show GCN5/PCAF and GCN5/PCAF-mediated H3K9ac correlate with, but are surprisingly dispensable for, NR target gene activation. In contrast, CBP/p300 and their HAT activities are essential for ligand-induced Pol II recruitment on, and activation of, NR target genes. These results highlight the substrate and site specificities of HATs in cells, demonstrate the distinct roles of GCN5/PCAF- and CBP/p300-mediated histone acetylations in gene activation, and suggest an important role of CBP/p300-mediated H3K18/27ac in NR-dependent transcription.
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              Acetylation of non-histone proteins modulates cellular signalling at multiple levels.

              Stephanie Spange, Tobias Wagner, Thorsten Heinzel … (2009)
              This review focuses on the posttranslational acetylation of non-histone proteins, which determines vital regulatory processes. The recruitment of histone acetyltransferases and histone deacetylases to the transcriptional machinery is a key element in the dynamic regulation of genes controlling cellular proliferation and differentiation. A steadily growing number of identified acetylated non-histone proteins demonstrate that reversible lysine acetylation affects mRNA stability, and the localisation, interaction, degradation and function of proteins. Interestingly, most non-histone proteins targeted by acetylation are relevant for tumourigenesis, cancer cell proliferation and immune functions. Therefore inhibitors of histone deacetylases are considered as candidate drugs for cancer therapy. Histone deacetylase inhibitors alter histone acetylation and chromatin structure, which modulates gene expression, as well as promoting the acetylation of non-histone proteins. Here, we summarise the complex effects of dynamic alterations in the cellular acetylome on physiologically relevant pathways.
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                Author and article information

                Contributors
                Anthony Lemarié: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 10 September 2015
                Publication date Collection: September 2015
                Volume: 16
                Issue: 9
                Pages: 21897-21910
                Affiliations
                [1 ]Department of Pathology, Affiliated Chenggong Hospital, Xiamen University, Xiamen 361000, China; E-Mails: liukun0309@ 123456163.com (K.L.); bioods@ 123456163.com (Q.Z.); mpf1314@ 123456126.com (P.M.); vivishao@ 123456foxmail.com (W.S.); luckydan100@ 123456126.com (D.L.); yws_huoyun@ 123456126.com (W.Y.); xmlinzhen@ 123456139.com (Z.L.); linqingyuan2007@ 123456163.com (Q.L.)
                [2 ]Chinese People’s Liberation Army No. 174 Clinical College, Anhui Medical University, Xiamen 361000, China; E-Mail: lotionmian@ 123456163.com
                [3 ]Department of Oncology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu 610072, China; E-Mail: lanht@ 123456sina.com
                Author notes
                [†]

                These authors contributed equally to this work.

                [* ]Author to whom correspondence should be addressed; E-Mail: skysea_ji@ 123456sina.com ; Tel./Fax: +86-59-2633-5744.
                Article
                Publisher ID: ijms-16-21897
                DOI: 10.3390/ijms160921897
                PMC ID: 4613287
                PubMed ID: 26378521
                SO-VID: 671c4445-c01d-4a78-8678-a646c9ed4898
                Copyright © © 2015 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 April 2015
                Date accepted : 31 August 2015
                Categories
                Subject: Article

                ScienceOpen disciplines: Molecular biology
                Keywords: gcn5,cell proliferation,cell invasion,stat3
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: gcn5, cell proliferation, cell invasion, stat3

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