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SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma

PURPOSE: Cytoskeleton is critical for carcinoma cell proliferation, migration, and invasion. Sad-1 and UNC-84 domain containing 1 (SUN1) is one of the core linkers of nucleoskeleton and cytoskeleton. However, the functions of SUN1 in lung adenocarcinoma are largely unknown. METHODS: In this study, w...

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Autores principales: Huang, Weiyi, Huang, Haihua, Wang, Lei, Hu, Jiong, Song, Weifeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5476752/
https://www.ncbi.nlm.nih.gov/pubmed/28652764
http://dx.doi.org/10.2147/OTT.S79727
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author Huang, Weiyi
Huang, Haihua
Wang, Lei
Hu, Jiong
Song, Weifeng
author_facet Huang, Weiyi
Huang, Haihua
Wang, Lei
Hu, Jiong
Song, Weifeng
author_sort Huang, Weiyi
collection PubMed
description PURPOSE: Cytoskeleton is critical for carcinoma cell proliferation, migration, and invasion. Sad-1 and UNC-84 domain containing 1 (SUN1) is one of the core linkers of nucleoskeleton and cytoskeleton. However, the functions of SUN1 in lung adenocarcinoma are largely unknown. METHODS: In this study, we first transduced the lentivirus delivering the short hairpin RNA (shRNA) against SUN1 to lung adenocarcinoma cells (A549 and 95D cells) with high efficiency. After lentivirus infection, quantitative real-time polymerase chain reaction and Western blotting were used to detect the expressions of SUN1 mRNA and protein. The cell proliferation and colony formation were detected by MTT assay and colony formation assay, respectively. The cell distribution in the cell cycle was analyzed by flow cytometry. RESULTS: Both mRNA and protein levels of SUN1 were significantly decreased in A549 and 95D cells after lentivirus infection, as indicated by quantitative real-time polymerase chain reaction and Western blot. Next, we found that cell proliferation and colony formation were markedly reduced in SUN1 silenced cells. Moreover, suppression of SUN1 led to cell cycle arrest at G0/G1 phase. Furthermore, Cyclin D1, CDK6, and CDK2 expressions were obviously reduced in A549 cells after SUN1 silencing. CONCLUSION: These results suggest that SUN1 plays an essential role in proliferation of lung adenocarcinoma cells in vitro and may be used as a potential therapeutic target for the treatment of lung adenocarcinoma in the future.
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spelling pubmed-54767522017-06-26 SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma Huang, Weiyi Huang, Haihua Wang, Lei Hu, Jiong Song, Weifeng Onco Targets Ther Original Research PURPOSE: Cytoskeleton is critical for carcinoma cell proliferation, migration, and invasion. Sad-1 and UNC-84 domain containing 1 (SUN1) is one of the core linkers of nucleoskeleton and cytoskeleton. However, the functions of SUN1 in lung adenocarcinoma are largely unknown. METHODS: In this study, we first transduced the lentivirus delivering the short hairpin RNA (shRNA) against SUN1 to lung adenocarcinoma cells (A549 and 95D cells) with high efficiency. After lentivirus infection, quantitative real-time polymerase chain reaction and Western blotting were used to detect the expressions of SUN1 mRNA and protein. The cell proliferation and colony formation were detected by MTT assay and colony formation assay, respectively. The cell distribution in the cell cycle was analyzed by flow cytometry. RESULTS: Both mRNA and protein levels of SUN1 were significantly decreased in A549 and 95D cells after lentivirus infection, as indicated by quantitative real-time polymerase chain reaction and Western blot. Next, we found that cell proliferation and colony formation were markedly reduced in SUN1 silenced cells. Moreover, suppression of SUN1 led to cell cycle arrest at G0/G1 phase. Furthermore, Cyclin D1, CDK6, and CDK2 expressions were obviously reduced in A549 cells after SUN1 silencing. CONCLUSION: These results suggest that SUN1 plays an essential role in proliferation of lung adenocarcinoma cells in vitro and may be used as a potential therapeutic target for the treatment of lung adenocarcinoma in the future. Dove Medical Press 2017-06-02 /pmc/articles/PMC5476752/ /pubmed/28652764 http://dx.doi.org/10.2147/OTT.S79727 Text en © 2017 Huang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Huang, Weiyi
Huang, Haihua
Wang, Lei
Hu, Jiong
Song, Weifeng
SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title_full SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title_fullStr SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title_full_unstemmed SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title_short SUN1 silencing inhibits cell growth through G0/G1 phase arrest in lung adenocarcinoma
title_sort sun1 silencing inhibits cell growth through g0/g1 phase arrest in lung adenocarcinoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5476752/
https://www.ncbi.nlm.nih.gov/pubmed/28652764
http://dx.doi.org/10.2147/OTT.S79727
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