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Title: Downregulation of HDAC9 inhibits cell proliferation and tumor formation by inducing cell cycle arrest in retinoblastoma

Abstract

Histone deacetylase 9 (HDAC9) is a member of class II HDACs, which regulates a wide variety of normal and abnormal physiological functions. Recently, HDAC9 has been found to be overexpressed in some types of human cancers. However, the role of HDAC9 in retinoblastoma remains unclear. In this study, we found that HDAC9 was commonly expressed in retinoblastoma tissues and HDAC9 was overexpressed in prognostically poor retinoblastoma patients. Through knocking down HDAC9 in Y79 and WERI-Rb-1 cells, the expression level of HDAC9 was found to be positively related to cell proliferation in vitro. Further investigation indicated that knockdown HDAC9 could significantly induce cell cycle arrest at G1 phase in retinoblastoma cells. Western blot assay showed downregulation of HDAC9 could significantly decrease cyclin E2 and CDK2 expression. Lastly, xenograft study in nude mice showed that downregulation of HDAC9 inhibited tumor growth and development in vivo. Therefore, our results suggest that HDAC9 could serve as a novel potential therapeutic target in the treatment of retinoblastoma. - Highlights: • High expression of HDAC9 correlates with poor patient prognosis. • Downregulation of HDAC9 inhibits cell proliferation in retinoblastoma cells. • Downregulation of HDAC9 induces cell cycle arrest at G1 phase in retinoblastoma cells. • Downregulation of HDAC9more » suppresses tumor growth in nude mice.« less

Authors:
; ; ; ;  [1];  [2];  [1]
  1. Medical School of Nanjing University, Department of Ophthalmology, Jinling Hospital, Nanjing, 210002 (China)
  2. State Key Laboratory of Silkworm Genome Biology, Institute of Sericulture and Systems Biology, Southwest University, Chongqing, 400716 (China)
Publication Date:
OSTI Identifier:
22596369
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 473; Journal Issue: 2; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; CELL CYCLE; CELL PROLIFERATION; HISTONES; IN VITRO; IN VIVO; MICE; NEOPLASMS; PATIENTS; PLANT GROWTH

Citation Formats

Zhang, Yiting, Wu, Dan, Xia, Fengjie, Xian, Hongyu, Zhu, Xinyue, Cui, Hongjuan, E-mail: hcui@swu.edu.cn, and Huang, Zhenping, E-mail: huangzhenping19633@163.com. Downregulation of HDAC9 inhibits cell proliferation and tumor formation by inducing cell cycle arrest in retinoblastoma. United States: N. p., 2016. Web. doi:10.1016/J.BBRC.2016.03.129.
Zhang, Yiting, Wu, Dan, Xia, Fengjie, Xian, Hongyu, Zhu, Xinyue, Cui, Hongjuan, E-mail: hcui@swu.edu.cn, & Huang, Zhenping, E-mail: huangzhenping19633@163.com. Downregulation of HDAC9 inhibits cell proliferation and tumor formation by inducing cell cycle arrest in retinoblastoma. United States. doi:10.1016/J.BBRC.2016.03.129.
Zhang, Yiting, Wu, Dan, Xia, Fengjie, Xian, Hongyu, Zhu, Xinyue, Cui, Hongjuan, E-mail: hcui@swu.edu.cn, and Huang, Zhenping, E-mail: huangzhenping19633@163.com. Fri . "Downregulation of HDAC9 inhibits cell proliferation and tumor formation by inducing cell cycle arrest in retinoblastoma". United States. doi:10.1016/J.BBRC.2016.03.129.
@article{osti_22596369,
title = {Downregulation of HDAC9 inhibits cell proliferation and tumor formation by inducing cell cycle arrest in retinoblastoma},
author = {Zhang, Yiting and Wu, Dan and Xia, Fengjie and Xian, Hongyu and Zhu, Xinyue and Cui, Hongjuan, E-mail: hcui@swu.edu.cn and Huang, Zhenping, E-mail: huangzhenping19633@163.com},
abstractNote = {Histone deacetylase 9 (HDAC9) is a member of class II HDACs, which regulates a wide variety of normal and abnormal physiological functions. Recently, HDAC9 has been found to be overexpressed in some types of human cancers. However, the role of HDAC9 in retinoblastoma remains unclear. In this study, we found that HDAC9 was commonly expressed in retinoblastoma tissues and HDAC9 was overexpressed in prognostically poor retinoblastoma patients. Through knocking down HDAC9 in Y79 and WERI-Rb-1 cells, the expression level of HDAC9 was found to be positively related to cell proliferation in vitro. Further investigation indicated that knockdown HDAC9 could significantly induce cell cycle arrest at G1 phase in retinoblastoma cells. Western blot assay showed downregulation of HDAC9 could significantly decrease cyclin E2 and CDK2 expression. Lastly, xenograft study in nude mice showed that downregulation of HDAC9 inhibited tumor growth and development in vivo. Therefore, our results suggest that HDAC9 could serve as a novel potential therapeutic target in the treatment of retinoblastoma. - Highlights: • High expression of HDAC9 correlates with poor patient prognosis. • Downregulation of HDAC9 inhibits cell proliferation in retinoblastoma cells. • Downregulation of HDAC9 induces cell cycle arrest at G1 phase in retinoblastoma cells. • Downregulation of HDAC9 suppresses tumor growth in nude mice.},
doi = {10.1016/J.BBRC.2016.03.129},
journal = {Biochemical and Biophysical Research Communications},
number = 2,
volume = 473,
place = {United States},
year = {Fri Apr 29 00:00:00 EDT 2016},
month = {Fri Apr 29 00:00:00 EDT 2016}
}