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HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation
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
2015
DOI10.1002/pros.22888
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
WOS记录号WOS:000346073500004
项目编号7122183 ; 81372746
资助机构Beijing Natural Science Foundation ; National Natural Science Foundation
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54641
专题北京大学第一临床医学院_泌尿外科
北京大学第一临床医学院_放射治疗科
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
推荐引用方式
GB/T 7714
Su, Boxing,Shi, Bentao,Tang, Yuan,et al. HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation[J]. PROSTATE,2015,75(1):33-44.
APA Su, Boxing.,Shi, Bentao.,Tang, Yuan.,Guo, Zhongqiang.,Yu, Xi.,...&Zhou, Liqun.(2015).HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation.PROSTATE,75(1),33-44.
MLA Su, Boxing,et al."HMGN5 Knockdown Sensitizes Prostate Cancer Cells to Ionizing Radiation".PROSTATE 75.1(2015):33-44.
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