https://scholars.lib.ntu.edu.tw/handle/123456789/519542
標題: | Increased histone deacetylase activity involved in the suppressed invasion of cancer cells survived from ALA-mediated photodynamic treatment | 作者: | Li P.-T. Tsai Y.-J. MING-JEN LEE Chen C.-T. |
公開日期: | 2015 | 出版社: | MDPI AG | 卷: | 16 | 期: | 10 | 起(迄)頁: | 23994-24010 | 來源出版物: | International Journal of Molecular Sciences | 摘要: | Previously, we have found that cancer cells survived from 5-Aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) have abnormal mitochondrial function and suppressed cellular invasiveness. Here we report that both the mRNA expression level and enzymatic activity of histone deacetylase (HDAC) were elevated in the PDT-derived variants with dysfunctional mitochondria. The activated HDAC deacetylated histone H3 and further resulted in the reduced migration and invasion, which correlated with the reduced expression of the invasion-related genes, matrix metalloproteinase 9 (MMP9), paternally expressed gene 1 (PEG1), and miR-355, the intronic miRNA. Using chromatin immunoprecipitation, we further demonstrate the reduced amount of acetylated histone H3 on the promoter regions of MMP9 and PEG1, supporting the down-regulation of these two genes in PDT-derived variants. These results indicate that HDAC activation induced by mitochondrial dysfunction could modulate the cellular invasiveness and its related gene expression. This argument was further verified in the 51-10 cybrid cells with the 4977 bp mtDNA deletion and A375 ρ0 cells with depleted mitochondria. These results indicate that mitochondrial dysfunction might suppress tumor invasion through modulating histone acetylation. ? 2015 by the authors; licensee MDPI, Basel, Switzerland. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84944104871&doi=10.3390%2fijms161023994&partnerID=40&md5=1f98aad93e9209abd0e74ac01fef2d41 https://scholars.lib.ntu.edu.tw/handle/123456789/519542 |
ISSN: | 1661-6596 | DOI: | 10.3390/ijms161023994 | SDG/關鍵字: | acetyl coenzyme A; aminolevulinic acid; cytochrome c oxidase; E1A associated p300 protein; epidermal growth factor receptor; gelatinase B; histone acetyltransferase GCN5; histone acetyltransferase PCAF; histone deacetylase; histone deacetylase 1; histone deacetylase 2; histone deacetylase 3; histone H3; microRNA; microRNA 355; unclassified drug; aminolevulinic acid; azacitidine; gelatinase B; histone; histone deacetylase; histone deacetylase inhibitor; hydroxamic acid; mesoderm specific transcript protein; microRNA; MIRN355 microRNA, human; MMP9 protein, human; protein; trichostatin A; Article; cancer cell; cancer inhibition; cell invasion assay; cell migration assay; cell survival; chemiluminescence immunoassay; chromatin immunoprecipitation; controlled study; down regulation; enzyme activity; gene; histone acetylation; human; human cell; mitochondrial DNA depletion; mRNA expression assay; paternally expressed gene 1; photodynamic therapy; photodynamics; real time polymerase chain reaction; reverse transcription polymerase chain reaction; Western blotting; acetylation; biosynthesis; cell motion; genetics; metabolism; mitochondrion; pathology; photochemotherapy; physiology; procedures; promoter region; tumor cell line; tumor invasion; Acetylation; Aminolevulinic Acid; Azacitidine; Cell Line, Tumor; Cell Movement; Chromatin Immunoprecipitation; Histone Deacetylase Inhibitors; Histone Deacetylases; Histones; Humans; Hydroxamic Acids; Matrix Metalloproteinase 9; MicroRNAs; Mitochondria; Neoplasm Invasiveness; Photochemotherapy; Promoter Regions, Genetic; Proteins |
顯示於: | 醫學系 |
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