Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer

被引:34
作者
Yang, Chun [1 ]
Croteau, Stephane [2 ]
Hardy, Pierre [1 ]
机构
[1] Univ Montreal, CHU St Justine, Res Ctr, 3175 Cote Sainte Catherine,Room 2.17.004, Montreal, PQ H3T IC5, Canada
[2] Univ Montreal, Dept Med Pediat Pharmacol & Physiol, Montreal, PQ, Canada
基金
加拿大健康研究院;
关键词
Histone deacetylase (HDAC) 9; Myocyte enhancer-binding factor 2-interacting transcriptional repressor (MITR); Tumorigenesis; Cancer development; Signaling pathways; CELL CARCINOMA GROWTH; GENE-EXPRESSION; DOWN-REGULATION; BREAST-CANCER; TRANSCRIPTIONAL CONTROL; MICRORNA-17-92; CLUSTER; PANCREATIC-CANCER; POOR-PROGNOSIS; T-CELLS; PROMOTES;
D O I
10.1007/s13402-021-00626-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background HDAC9 (histone deacetylase 9) belongs to the class IIa family of histone deacetylases. This enzyme can shuttle freely between the nucleus and cytoplasm and promotes tissue-specific transcriptional regulation by interacting with histone and non-histone substrates. HDAC9 plays an essential role in diverse physiological processes including cardiac muscle development, bone formation, adipocyte differentiation and innate immunity. HDAC9 inhibition or activation is therefore a promising avenue for therapeutic intervention in several diseases. HDAC9 overexpression is also common in cancer cells, where HDAC9 alters the expression and activity of numerous relevant proteins involved in carcinogenesis. Conclusions This review summarizes the most recent discoveries regarding HDAC9 as a crucial regulator of specific physiological systems and, more importantly, highlights the diverse spectrum of HDAC9-mediated posttranslational modifications and their contributions to cancer pathogenesis. HDAC9 is a potential novel therapeutic target, and the restoration of aberrant expression patterns observed among HDAC9 target genes and their related signaling pathways may provide opportunities to the design of novel anticancer therapeutic strategies.
引用
收藏
页码:997 / 1017
页数:21
相关论文
共 152 条
[51]   Association with class IIa histone deacetylases upregulates the sumoylation of MEF2 transcription factors [J].
Grégoire, S ;
Yang, XJ .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (06) :2273-2287
[52]   Long noncoding RNA CBR3 antisense RNA 1 promotes the aggressive phenotypes of non-small-cell lung cancer by sponging microRNA-509-3p and competitively upregulating HDAC9 expression [J].
Guan, Yun ;
Yang, Juan ;
Liu, Xinmei ;
Chu, Lijuan .
ONCOLOGY REPORTS, 2020, 44 (04) :1403-1414
[53]   Aurora B-dependent Regulation of Class IIa Histone Deacetylases by Mitotic Nuclear Localization Signal Phosphorylation [J].
Guise, Amanda J. ;
Greco, Todd M. ;
Zhang, Irene Y. ;
Yu, Fang ;
Cristea, Ileana M. .
MOLECULAR & CELLULAR PROTEOMICS, 2012, 11 (11) :1220-1229
[54]   Regulation of HDAC9 gene expression by MEF2 establishes a negative-feedback loop in the transcriptional circuitry of muscle differentiation [J].
Haberland, Michael ;
Arnold, Michael A. ;
McAnally, John ;
Phan, Dillon ;
Kim, Yuri ;
Olson, Eric N. .
MOLECULAR AND CELLULAR BIOLOGY, 2007, 27 (02) :518-525
[55]   The many roles of histone deacetylases in development and physiology: implications for disease and therapy [J].
Haberland, Michael ;
Montgomery, Rusty L. ;
Olson, Eric N. .
NATURE REVIEWS GENETICS, 2009, 10 (01) :32-42
[56]  
Han X, 2016, FRONT BIOSCI-LANDMRK, V21, P907
[57]   Protein kinase C-related kinase targets nuclear localization signals in a subset of class IIa histone deacetylases [J].
Harrison, Brooke C. ;
Huynh, Khai ;
Lundgaard, Greta L. ;
Helmke, Steven M. ;
Perryman, M. Benjamin ;
McKinsey, Timothy A. .
FEBS LETTERS, 2010, 584 (06) :1103-1110
[58]   A role for histone deacetylase activity in HDAC1-mediated transcriptional repression [J].
Hassig, CA ;
Tong, JK ;
Fleischer, TC ;
Owa, T ;
Grable, PG ;
Ayer, DE ;
Schreiber, SL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (07) :3519-3524
[59]  
Hattori Y, 2007, INT J ONCOL, V30, P1427
[60]  
Hu SQ, 2020, DIABETES METAB J, V44, P234