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LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis
BACKGROUND: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC. METHODS: Sixty-four HCC pati...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7652235/ https://www.ncbi.nlm.nih.gov/pubmed/33177878 http://dx.doi.org/10.2147/CMAR.S254950 |
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author | Cui, Dan Ni, Caifang |
author_facet | Cui, Dan Ni, Caifang |
author_sort | Cui, Dan |
collection | PubMed |
description | BACKGROUND: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC. METHODS: Sixty-four HCC patients were enrolled and followed up for 5 years to analyze the prognostic value of Lnc712 for HCC. HCC cells were transfected with Lnc712 expression vector, Bach-1 expression vector (or siRNA) and miR-142-3p mimic (or inhibitor) to explore the interactions among Lnc712, miR-142-3p and Bach-1. Cell proliferation, migration, invasion and cell cycle were analyzed by CCK-8 assay, transwell assay, wound healing assay and flow cytometry assay, respectively. RESULTS: The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients. In HCC cells, Lnc712 interacted with miR-142-3p and upregulated Bach-1, a target of miR-142-3p. In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic. Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice. CONCLUSION: Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis. |
format | Online Article Text |
id | pubmed-7652235 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-76522352020-11-10 LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis Cui, Dan Ni, Caifang Cancer Manag Res Original Research BACKGROUND: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC. METHODS: Sixty-four HCC patients were enrolled and followed up for 5 years to analyze the prognostic value of Lnc712 for HCC. HCC cells were transfected with Lnc712 expression vector, Bach-1 expression vector (or siRNA) and miR-142-3p mimic (or inhibitor) to explore the interactions among Lnc712, miR-142-3p and Bach-1. Cell proliferation, migration, invasion and cell cycle were analyzed by CCK-8 assay, transwell assay, wound healing assay and flow cytometry assay, respectively. RESULTS: The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients. In HCC cells, Lnc712 interacted with miR-142-3p and upregulated Bach-1, a target of miR-142-3p. In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic. Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice. CONCLUSION: Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis. Dove 2020-11-05 /pmc/articles/PMC7652235/ /pubmed/33177878 http://dx.doi.org/10.2147/CMAR.S254950 Text en © 2020 Cui and Ni. 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 Cui, Dan Ni, Caifang LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title | LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title_full | LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title_fullStr | LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title_full_unstemmed | LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title_short | LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis |
title_sort | lncrna lnc712 promotes tumorigenesis in hepatocellular carcinoma by targeting mir-142-3p/bach-1 axis |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7652235/ https://www.ncbi.nlm.nih.gov/pubmed/33177878 http://dx.doi.org/10.2147/CMAR.S254950 |
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