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Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop
Holliday Junction Recognition Protein (HJURP) is a centromeric histone chaperone involving in de novo histone H3 variant CenH3 (CENP-A) recruitment. Our transcriptome and in vivo study revealed that HJURP is significantly upregulated in bladder cancer (BCa) tissues at both mRNA and protein levels. K...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Ivyspring International Publisher
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560147/ https://www.ncbi.nlm.nih.gov/pubmed/28819432 http://dx.doi.org/10.7150/jca.19967 |
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author | Cao, Rui Wang, Gang Qian, Kaiyu Chen, Liang Qian, Guofeng Xie, Conghua Dan, Han C. Jiang, Wei Wu, Min Wu, Chin-Lee Xiao, Yu Wang, Xinghuan |
author_facet | Cao, Rui Wang, Gang Qian, Kaiyu Chen, Liang Qian, Guofeng Xie, Conghua Dan, Han C. Jiang, Wei Wu, Min Wu, Chin-Lee Xiao, Yu Wang, Xinghuan |
author_sort | Cao, Rui |
collection | PubMed |
description | Holliday Junction Recognition Protein (HJURP) is a centromeric histone chaperone involving in de novo histone H3 variant CenH3 (CENP-A) recruitment. Our transcriptome and in vivo study revealed that HJURP is significantly upregulated in bladder cancer (BCa) tissues at both mRNA and protein levels. Knockdown of HJURP inhibited proliferation and viability of BCa cell lines revealed by CCK-8, colony formation and Ki-67-staining assays, and induced apoptosis and reactive oxygen species (ROS) production, as well as triggered cell cycle arrest at G0/G1 phase possibly via loss of CENP-A. Interestingly, in the HJURP-reduced BCa cells the levels of PPARγ and acetylated-p53 were increased, while the ratio of phosphorylated/total SIRT1 protein was decreased. Moreover, after treatment of the BCa cells using PPARγ antagonist (GW9662) and SIRT1 agonist (resveratrol, RSV) respectively, thee phenotypes of cell cycle arrest, increased ROS production and inhibited proliferation rate were all rescued. Taken together, our results suggested that HJURP might regulate proliferation and apoptosis via the PPARγ-SIRT1 negative feedback loop in BCa cells. |
format | Online Article Text |
id | pubmed-5560147 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-55601472017-08-17 Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop Cao, Rui Wang, Gang Qian, Kaiyu Chen, Liang Qian, Guofeng Xie, Conghua Dan, Han C. Jiang, Wei Wu, Min Wu, Chin-Lee Xiao, Yu Wang, Xinghuan J Cancer Research Paper Holliday Junction Recognition Protein (HJURP) is a centromeric histone chaperone involving in de novo histone H3 variant CenH3 (CENP-A) recruitment. Our transcriptome and in vivo study revealed that HJURP is significantly upregulated in bladder cancer (BCa) tissues at both mRNA and protein levels. Knockdown of HJURP inhibited proliferation and viability of BCa cell lines revealed by CCK-8, colony formation and Ki-67-staining assays, and induced apoptosis and reactive oxygen species (ROS) production, as well as triggered cell cycle arrest at G0/G1 phase possibly via loss of CENP-A. Interestingly, in the HJURP-reduced BCa cells the levels of PPARγ and acetylated-p53 were increased, while the ratio of phosphorylated/total SIRT1 protein was decreased. Moreover, after treatment of the BCa cells using PPARγ antagonist (GW9662) and SIRT1 agonist (resveratrol, RSV) respectively, thee phenotypes of cell cycle arrest, increased ROS production and inhibited proliferation rate were all rescued. Taken together, our results suggested that HJURP might regulate proliferation and apoptosis via the PPARγ-SIRT1 negative feedback loop in BCa cells. Ivyspring International Publisher 2017-07-20 /pmc/articles/PMC5560147/ /pubmed/28819432 http://dx.doi.org/10.7150/jca.19967 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper Cao, Rui Wang, Gang Qian, Kaiyu Chen, Liang Qian, Guofeng Xie, Conghua Dan, Han C. Jiang, Wei Wu, Min Wu, Chin-Lee Xiao, Yu Wang, Xinghuan Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title | Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title_full | Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title_fullStr | Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title_full_unstemmed | Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title_short | Silencing of HJURP induces dysregulation of cell cycle and ROS metabolism in bladder cancer cells via PPARγ-SIRT1 feedback loop |
title_sort | silencing of hjurp induces dysregulation of cell cycle and ros metabolism in bladder cancer cells via pparγ-sirt1 feedback loop |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560147/ https://www.ncbi.nlm.nih.gov/pubmed/28819432 http://dx.doi.org/10.7150/jca.19967 |
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