北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第一临床医学院  > 泌尿外科  > 期刊论文
学科主题: 临床医学
题名:
HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation
作者: Su, Boxing1,2,3; Shi, Bentao4; Tang, Yuan1,2,3; Guo, Zhongqiang1,2,3; Yu, Xi1,2,3; He, Xinyong5; Li, Xuesong1,2,3; Gao, Xianshu5; Zhou, Liqun1,2,3
关键词: prostate cancer ; high mobility group N 5 (HMGN5) ; ionizing radiation
刊名: PROSTATE
发表日期: 2015
DOI: 10.1002/pros.22888
卷: 75, 期:1, 页:33-44
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism ; Urology & Nephrology
研究领域[WOS]: Endocrinology & Metabolism ; Urology & Nephrology
关键词[WOS]: CHROMOSOMAL-PROTEIN HMGN1 ; MOBILITY-GROUP PROTEINS ; BCL-2 FAMILY PROTEINS ; DOUBLE-STRAND BREAKS ; REACTIVE OXYGEN ; GENE-EXPRESSION ; DNA-REPAIR ; KAPPA-B ; FUTURE-DIRECTIONS ; INDUCED APOPTOSIS
英文摘要:

BACKGROUNDHigh Mobility Group N (HMGN) proteins are a family of chromatin structural proteins that specifically bind to nucleosome core particles. HMGN5 is a novel and characteristic member of the HMGN protein family. We have previously found that HMGN5 is upregulated in prostate cancer and its downregulation had been demonstrated to induce apoptosis and G2-M cell cycle arrest.

METHODSThe radiosensitization effect of HMGN5 knockdown on PC3 and DU145 cells was assessed using clonogenic assay, flow cytometry, and comet assay. The DNA double-strand break (DSB) repair kinetics of HMGN5 knockdown and control cells after radiation exposure was evaluated using immunocytofluorescence. The mitochondrial reactive oxygen species (ROS) levels were estimated using Dihydrorhodamine 123 (DHR 123) probes. Expression of mitochondrial antioxidant MnSOD was measured by real-time PCR and Western blot. The expression of antiapoptotic proteins Bcl-2 and Bcl-xL as well as cleavage of caspase-3, caspase-9, and PARP were also measured using Western blot.

RESULTSHMGN5 knockdown cells exhibit decreased clonogenic survival and increased apoptosis rate in response to 2-8 Gy ionizing radiation (IR). Loss of HMGN5 does not affect the DSB repair kinetics after radiation exposure. HMGN5 knockdown cells demonstrated increased mitochondrial ROS level and suppressed induction of MnSOD upon radiation compared with control cells upon radiation. Further, MnSOD knockdown resulted in inhibited cell viability as well as increased mitochondrial ROS level and apoptosis upon radiation in PC3 and DU145 cells. Finally, HMGN5 knockdown cells showed significantly decreased levels of antiapoptotic proteins Bcl-2 and Bcl-xL as well as increased cleavage of caspase-3, caspase-9, and PARP compared with control cells after radiation.

CONCLUSIONSHMGN5 knockdown sensitizes prostate cancer cells to ionizing radiation, and the radiosensitization effect may be partially mediated through suppressed induction of MnSOD and enhanced activation of apoptosis pathway in response to IR. Prostate 75:33-44, 2015. (c) 2014 Wiley Periodicals, Inc.

语种: 英语
所属项目编号: 7122183 ; 81372746
项目资助者: Beijing Natural Science Foundation ; National Natural Science Foundation
WOS记录号: WOS:000346073500004
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54641
Appears in Collections:北京大学第一临床医学院_泌尿外科_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.Peking Univ, Hosp 1, Dept Urol, Beijing 100034, Peoples R China
2.Peking Univ, Inst Urol, Beijing 100034, Peoples R China
3.Natl Urol Canc Ctr, Beijing, Peoples R China
4.Peking Univ, Shenzhen Hosp, Dept Urol, Shenzhen, Guangdong, Peoples R China
5.Peking Univ, Hosp 1, Dept Radiat Oncol, Beijing 100034, Peoples R China

Recommended Citation:
Su, Boxing,Shi, Bentao,Tang, Yuan,et al. HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation[J]. PROSTATE,2015,75(1):33-44.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Su, Boxing]'s Articles
[Shi, Bentao]'s Articles
[Tang, Yuan]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Su, Boxing]‘s Articles
[Shi, Bentao]‘s Articles
[Tang, Yuan]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace