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CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p
BACKGROUND: Numerous circular RNAs (circRNAs) are functionally investigated in various human cancers, including colorectal cancer (CRC). In this study, we explored the function of circCSNK1G1 and mechanism of action in CRC, aiming to provide evidence for circCSNK1G1 involving in CRC pathogenesis. ME...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538009/ https://www.ncbi.nlm.nih.gov/pubmed/33061642 http://dx.doi.org/10.2147/CMAR.S262007 |
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author | Huang, Xianming Shen, Xiaohua Peng, Lixiang Mai, Wenli Wan, Yiye Zhang, Huiqing |
author_facet | Huang, Xianming Shen, Xiaohua Peng, Lixiang Mai, Wenli Wan, Yiye Zhang, Huiqing |
author_sort | Huang, Xianming |
collection | PubMed |
description | BACKGROUND: Numerous circular RNAs (circRNAs) are functionally investigated in various human cancers, including colorectal cancer (CRC). In this study, we explored the function of circCSNK1G1 and mechanism of action in CRC, aiming to provide evidence for circCSNK1G1 involving in CRC pathogenesis. METHODS: The expression of circCSNK1G1, miR-455-3p and Myosin VI (MYO6) were examined using quantitative real-time polymerase chain reaction (qRT-PCR). The functions of circCSNK1G1 on cell proliferation, apoptosis, cycle and migration/invasion were investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry assay and transwell assay, respectively. The targeted relationship between miR-455-3p and circCSNK1G1 or MYO6 predicted by bioinformatics analysis was validated using dual-luciferase reporter assay and RNA pull-down assay. The role of circCSNK1G1 was also explored in nude mice in vivo. RESULTS: The expression of circCSNK1G1 and MYO6 was elevated, while the expression of miR-455-3p was declined in CRC tissues and cells. Silencing circCSNK1G1 inhibited CRC cell proliferation, migration and invasion and induced cell apoptosis and cell cycle arrest. MiR-455-3p was a target of circCSNK1G1, and miR-455-3p could bind to MYO6. CircCSNK1G1 positively regulated MYO6 expression by targeting miR-455-3p. Inhibition of miR-455-3p reversed the effects of circCSNK1G1 silencing in CRC cells. Besides, miR-455-3p restoration blocked CRC cell growth and metastasis, which were abolished by MYO6 overexpression. Moreover, circCSNK1G1 regulated the miR-455-3p/MYO6 axis to block tumor growth in vivo. CONCLUSION: CircCSNK1G1 participated in the progression of CRC partly by modulating the miR-455-3p/MYO6 network, which provided a theoretical basis for circCSNK1G1 involving in CRC pathogenesis, hinting that circCSNK1G1 might be a useful biomarker for CRC treatment. |
format | Online Article Text |
id | pubmed-7538009 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-75380092020-10-14 CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p Huang, Xianming Shen, Xiaohua Peng, Lixiang Mai, Wenli Wan, Yiye Zhang, Huiqing Cancer Manag Res Original Research BACKGROUND: Numerous circular RNAs (circRNAs) are functionally investigated in various human cancers, including colorectal cancer (CRC). In this study, we explored the function of circCSNK1G1 and mechanism of action in CRC, aiming to provide evidence for circCSNK1G1 involving in CRC pathogenesis. METHODS: The expression of circCSNK1G1, miR-455-3p and Myosin VI (MYO6) were examined using quantitative real-time polymerase chain reaction (qRT-PCR). The functions of circCSNK1G1 on cell proliferation, apoptosis, cycle and migration/invasion were investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry assay and transwell assay, respectively. The targeted relationship between miR-455-3p and circCSNK1G1 or MYO6 predicted by bioinformatics analysis was validated using dual-luciferase reporter assay and RNA pull-down assay. The role of circCSNK1G1 was also explored in nude mice in vivo. RESULTS: The expression of circCSNK1G1 and MYO6 was elevated, while the expression of miR-455-3p was declined in CRC tissues and cells. Silencing circCSNK1G1 inhibited CRC cell proliferation, migration and invasion and induced cell apoptosis and cell cycle arrest. MiR-455-3p was a target of circCSNK1G1, and miR-455-3p could bind to MYO6. CircCSNK1G1 positively regulated MYO6 expression by targeting miR-455-3p. Inhibition of miR-455-3p reversed the effects of circCSNK1G1 silencing in CRC cells. Besides, miR-455-3p restoration blocked CRC cell growth and metastasis, which were abolished by MYO6 overexpression. Moreover, circCSNK1G1 regulated the miR-455-3p/MYO6 axis to block tumor growth in vivo. CONCLUSION: CircCSNK1G1 participated in the progression of CRC partly by modulating the miR-455-3p/MYO6 network, which provided a theoretical basis for circCSNK1G1 involving in CRC pathogenesis, hinting that circCSNK1G1 might be a useful biomarker for CRC treatment. Dove 2020-10-02 /pmc/articles/PMC7538009/ /pubmed/33061642 http://dx.doi.org/10.2147/CMAR.S262007 Text en © 2020 Huang et al. http://creativecommons.org/licenses/by-nc/3.0/ 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Huang, Xianming Shen, Xiaohua Peng, Lixiang Mai, Wenli Wan, Yiye Zhang, Huiqing CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title | CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title_full | CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title_fullStr | CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title_full_unstemmed | CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title_short | CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p |
title_sort | circcsnk1g1 contributes to the development of colorectal cancer by increasing the expression of myo6 via competitively targeting mir-455-3p |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538009/ https://www.ncbi.nlm.nih.gov/pubmed/33061642 http://dx.doi.org/10.2147/CMAR.S262007 |
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