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LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143

BACKGROUND: Long noncoding RNAs (lncRNAs) play critical and complex roles in regulating various biological processes of cancers. Our study aimed to investigate the involvement of lncRNA NCK1-AS1 in urinary bladder cancer (UBC). METHODS: qRT-PCR was used to detect the expression of lncRNA NCK1-AS1 an...

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Autores principales: Qiao, Zhongjie, Dai, Hongshuang, Zhang, Yunzhu, Li, Qiang, Zhao, Meng, Yue, Tongyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064288/
https://www.ncbi.nlm.nih.gov/pubmed/32184669
http://dx.doi.org/10.2147/CMAR.S223172
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author Qiao, Zhongjie
Dai, Hongshuang
Zhang, Yunzhu
Li, Qiang
Zhao, Meng
Yue, Tongyun
author_facet Qiao, Zhongjie
Dai, Hongshuang
Zhang, Yunzhu
Li, Qiang
Zhao, Meng
Yue, Tongyun
author_sort Qiao, Zhongjie
collection PubMed
description BACKGROUND: Long noncoding RNAs (lncRNAs) play critical and complex roles in regulating various biological processes of cancers. Our study aimed to investigate the involvement of lncRNA NCK1-AS1 in urinary bladder cancer (UBC). METHODS: qRT-PCR was used to detect the expression of lncRNA NCK1-AS1 and miR-143 in UBC tissues and cells. The dual-luciferase reporter system assays were used to confirm the interaction between NCK1-AS1 and miR-143, and flow cytometry assays were applied to examine the behavioral changes in HT-1376 and HT-1197 cell lines. RESULTS: It was observed that NCK1-AS1 was up-regulated, while miR-143 was down-regulated in tumor tissues than in adjacent healthy tissues of urinary bladder cancer (UBC) patients. A 5-year survival analysis showed that the survival rate of patients with high NCK1-AS1 level or low miR-143 level in tumor tissues appears relatively low. Correlation analysis revealed a significant inverse correlation between NCK1-AS1 and miR-143 in tumor tissues. Over-expression NCK1-AS1 reduced the expression level of miR-143, while elevating the level of miR-143 failed to affect NCK1-AS1 expression. NCK1-AS1 over-expression led to promoted proliferation and increased percentage of CD133+ (stemness) cells. CONCLUSION: Therefore, NCK1-AS1 promotes cancer cell proliferation and increases cell stemness in UBC patients by down-regulating miR-143.
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spelling pubmed-70642882020-03-17 LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143 Qiao, Zhongjie Dai, Hongshuang Zhang, Yunzhu Li, Qiang Zhao, Meng Yue, Tongyun Cancer Manag Res Original Research BACKGROUND: Long noncoding RNAs (lncRNAs) play critical and complex roles in regulating various biological processes of cancers. Our study aimed to investigate the involvement of lncRNA NCK1-AS1 in urinary bladder cancer (UBC). METHODS: qRT-PCR was used to detect the expression of lncRNA NCK1-AS1 and miR-143 in UBC tissues and cells. The dual-luciferase reporter system assays were used to confirm the interaction between NCK1-AS1 and miR-143, and flow cytometry assays were applied to examine the behavioral changes in HT-1376 and HT-1197 cell lines. RESULTS: It was observed that NCK1-AS1 was up-regulated, while miR-143 was down-regulated in tumor tissues than in adjacent healthy tissues of urinary bladder cancer (UBC) patients. A 5-year survival analysis showed that the survival rate of patients with high NCK1-AS1 level or low miR-143 level in tumor tissues appears relatively low. Correlation analysis revealed a significant inverse correlation between NCK1-AS1 and miR-143 in tumor tissues. Over-expression NCK1-AS1 reduced the expression level of miR-143, while elevating the level of miR-143 failed to affect NCK1-AS1 expression. NCK1-AS1 over-expression led to promoted proliferation and increased percentage of CD133+ (stemness) cells. CONCLUSION: Therefore, NCK1-AS1 promotes cancer cell proliferation and increases cell stemness in UBC patients by down-regulating miR-143. Dove 2020-03-06 /pmc/articles/PMC7064288/ /pubmed/32184669 http://dx.doi.org/10.2147/CMAR.S223172 Text en © 2020 Qiao 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
Qiao, Zhongjie
Dai, Hongshuang
Zhang, Yunzhu
Li, Qiang
Zhao, Meng
Yue, Tongyun
LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title_full LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title_fullStr LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title_full_unstemmed LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title_short LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143
title_sort lncrna nck1-as1 promotes cancer cell proliferation and increase cell stemness in urinary bladder cancer patients by downregulating mir-143
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064288/
https://www.ncbi.nlm.nih.gov/pubmed/32184669
http://dx.doi.org/10.2147/CMAR.S223172
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