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Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells
NIMA-related kinase-7 (Nek7) is a centrosomal kinase involved in various types of cancer, including gallbladder cancer and hepatocellular carcinoma. However, the biological function and the potential underlying mechanism of Nek7 in retinoblastoma remain largely unknown. Therefore, the present study...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774400/ https://www.ncbi.nlm.nih.gov/pubmed/29434721 http://dx.doi.org/10.3892/etm.2017.5558 |
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author | Zhang, Jian Wang, Li Zhang, Yongkang |
author_facet | Zhang, Jian Wang, Li Zhang, Yongkang |
author_sort | Zhang, Jian |
collection | PubMed |
description | NIMA-related kinase-7 (Nek7) is a centrosomal kinase involved in various types of cancer, including gallbladder cancer and hepatocellular carcinoma. However, the biological function and the potential underlying mechanism of Nek7 in retinoblastoma remain largely unknown. Therefore, the present study investigated the effects of Nek7 in retinoblastoma cells. The expression of Nek7 was initially determined and observed to be commonly upregulated in retinoblastoma cell lines (Y79, SO-RB50 and WERI-RB1) as compared with that in normal retinal pigment epithelium cells. Next, the endogenous expression of Nek7 was efficiently knocked down in Y79 and SO-RB50 cells using a lentivirus-mediated RNA interference approach, as confirmed by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Loss-of-function assays, including MTT, colony formation and flow cytometry, indicated that knockdown of Nek7 significantly inhibited cell growth, impaired the colony formation ability and induced cell cycle arrest at G0/G1 phase. Furthermore, mechanistic studies demonstrated that silencing of Nek7 resulted in reduced cyclin-dependent kinase 2, cyclin D1 and cyclin E levels in vitro. In conclusion, the present study highlights the crucial role of Nek7 in promoting retinoblastoma cell proliferation, and Nek7-silencing may serve as a novel therapeutic target for retinoblastoma. |
format | Online Article Text |
id | pubmed-5774400 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57744002018-02-12 Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells Zhang, Jian Wang, Li Zhang, Yongkang Exp Ther Med Articles NIMA-related kinase-7 (Nek7) is a centrosomal kinase involved in various types of cancer, including gallbladder cancer and hepatocellular carcinoma. However, the biological function and the potential underlying mechanism of Nek7 in retinoblastoma remain largely unknown. Therefore, the present study investigated the effects of Nek7 in retinoblastoma cells. The expression of Nek7 was initially determined and observed to be commonly upregulated in retinoblastoma cell lines (Y79, SO-RB50 and WERI-RB1) as compared with that in normal retinal pigment epithelium cells. Next, the endogenous expression of Nek7 was efficiently knocked down in Y79 and SO-RB50 cells using a lentivirus-mediated RNA interference approach, as confirmed by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Loss-of-function assays, including MTT, colony formation and flow cytometry, indicated that knockdown of Nek7 significantly inhibited cell growth, impaired the colony formation ability and induced cell cycle arrest at G0/G1 phase. Furthermore, mechanistic studies demonstrated that silencing of Nek7 resulted in reduced cyclin-dependent kinase 2, cyclin D1 and cyclin E levels in vitro. In conclusion, the present study highlights the crucial role of Nek7 in promoting retinoblastoma cell proliferation, and Nek7-silencing may serve as a novel therapeutic target for retinoblastoma. D.A. Spandidos 2018-02 2017-11-23 /pmc/articles/PMC5774400/ /pubmed/29434721 http://dx.doi.org/10.3892/etm.2017.5558 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhang, Jian Wang, Li Zhang, Yongkang Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title | Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title_full | Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title_fullStr | Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title_full_unstemmed | Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title_short | Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
title_sort | downregulation of nima-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774400/ https://www.ncbi.nlm.nih.gov/pubmed/29434721 http://dx.doi.org/10.3892/etm.2017.5558 |
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