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shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells
BACKGROUND: Polo-like kinase 1 (PLK1) is a serine/threonine protein kinase, which has been studied as a potential gene therapy target for many years. PLK1 is overexpressed in a variety of tumors, and its expression often negatively correlated with patient prognosis. However, the role of PLK1 in naso...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798612/ https://www.ncbi.nlm.nih.gov/pubmed/35117900 http://dx.doi.org/10.21037/tcr-20-811 |
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author | Zhou, Yan Wu, Chu Liu, Bingxue Zhu, Juan Zhong, Yating Yuan, Yuqing Huang, Yue Tang, Yunlian |
author_facet | Zhou, Yan Wu, Chu Liu, Bingxue Zhu, Juan Zhong, Yating Yuan, Yuqing Huang, Yue Tang, Yunlian |
author_sort | Zhou, Yan |
collection | PubMed |
description | BACKGROUND: Polo-like kinase 1 (PLK1) is a serine/threonine protein kinase, which has been studied as a potential gene therapy target for many years. PLK1 is overexpressed in a variety of tumors, and its expression often negatively correlated with patient prognosis. However, the role of PLK1 in nasopharyngeal carcinoma (NPC) is rarely studied. METHODS: Two recombinant vector plasmids were transfected into CNE2 cell lines by liposome transfection, CNE2/PLK1 shRNA target PLK1 mRNA, as well as a non-targeting control plasmid, CNE2/NC shRNA. Meanwhile, non-transfected cells (CNE2) were also used as controls. Real-time quantitative PCR (qRT-PCR) and Western blotting were performed to detect the transfection effect. The effects of the downregulation of PLK1 on cell biological behavior was evaluated in vitro by using CCK8, Transwell, colony-forming and flow-cytometry assays. RESULTS: PLK1 mRNA and protein were significantly inhibited in CNE2/PLK1 shRNA cells. Compared to control groups, the CNE2/PLK1 shRNA cells showed slower cell growth and a significantly decreased cell-cloning rate. Both migration and invasion were significantly inhibited in experimental cells. The proportions of G2-phase and apoptotic cells within the experimental group were significantly increased. CONCLUSIONS: Our results indicate that specific interference of PLK1 gene expression can significantly inhibit the proliferation and invasion of NPC (CNE2) cells. |
format | Online Article Text |
id | pubmed-8798612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87986122022-02-02 shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells Zhou, Yan Wu, Chu Liu, Bingxue Zhu, Juan Zhong, Yating Yuan, Yuqing Huang, Yue Tang, Yunlian Transl Cancer Res Original Article BACKGROUND: Polo-like kinase 1 (PLK1) is a serine/threonine protein kinase, which has been studied as a potential gene therapy target for many years. PLK1 is overexpressed in a variety of tumors, and its expression often negatively correlated with patient prognosis. However, the role of PLK1 in nasopharyngeal carcinoma (NPC) is rarely studied. METHODS: Two recombinant vector plasmids were transfected into CNE2 cell lines by liposome transfection, CNE2/PLK1 shRNA target PLK1 mRNA, as well as a non-targeting control plasmid, CNE2/NC shRNA. Meanwhile, non-transfected cells (CNE2) were also used as controls. Real-time quantitative PCR (qRT-PCR) and Western blotting were performed to detect the transfection effect. The effects of the downregulation of PLK1 on cell biological behavior was evaluated in vitro by using CCK8, Transwell, colony-forming and flow-cytometry assays. RESULTS: PLK1 mRNA and protein were significantly inhibited in CNE2/PLK1 shRNA cells. Compared to control groups, the CNE2/PLK1 shRNA cells showed slower cell growth and a significantly decreased cell-cloning rate. Both migration and invasion were significantly inhibited in experimental cells. The proportions of G2-phase and apoptotic cells within the experimental group were significantly increased. CONCLUSIONS: Our results indicate that specific interference of PLK1 gene expression can significantly inhibit the proliferation and invasion of NPC (CNE2) cells. AME Publishing Company 2020-09 /pmc/articles/PMC8798612/ /pubmed/35117900 http://dx.doi.org/10.21037/tcr-20-811 Text en 2020 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/. |
spellingShingle | Original Article Zhou, Yan Wu, Chu Liu, Bingxue Zhu, Juan Zhong, Yating Yuan, Yuqing Huang, Yue Tang, Yunlian shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title | shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title_full | shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title_fullStr | shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title_full_unstemmed | shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title_short | shRNA targeting PLK1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
title_sort | shrna targeting plk1 inhibits the proliferation and invasion of nasopharyngeal carcinoma cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798612/ https://www.ncbi.nlm.nih.gov/pubmed/35117900 http://dx.doi.org/10.21037/tcr-20-811 |
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