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LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4

BACKGROUND: Mounting evidences have indicated that long non-coding RNA (lncRNA) HOXD cluster antisense RNA 1 (HOXD-AS1) is dysregulated and participates into the progression of cancers. This study aims to investigate the biological roles and mechanisms of HOXD-AS1 in the metastasis of hepatocellular...

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Autores principales: Ji, Wenbin, Wang, Qunfeng, Yang, Jian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216491/
https://www.ncbi.nlm.nih.gov/pubmed/32425696
http://dx.doi.org/10.1186/s12935-020-01217-8
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author Ji, Wenbin
Wang, Qunfeng
Yang, Jian
author_facet Ji, Wenbin
Wang, Qunfeng
Yang, Jian
author_sort Ji, Wenbin
collection PubMed
description BACKGROUND: Mounting evidences have indicated that long non-coding RNA (lncRNA) HOXD cluster antisense RNA 1 (HOXD-AS1) is dysregulated and participates into the progression of cancers. This study aims to investigate the biological roles and mechanisms of HOXD-AS1 in the metastasis of hepatocellular carcinoma (HCC). METHODS: The quantitative real-time PCR (qPCR) assay was used to assess the level of miR-326 and HOXD-AS1 in HCC tissues and cell lines. The growth of HCC cell was analyzed by using CCK-8 assay and colony formation assay. The migration and invasion of HCC cell were investigated by using wound healing and transwell invasion analysis. The expressions of SLC27A4, N-cadherin and E-cadherin were determined by western blotting. The growth of HCC cell in vivo was assessed by using xenograft model. RESULTS: Here, we elaborated that HOXD-AS1 was overexpressed in HCC tissues than that in the adjacent normal tissues and the level of HOXD-AS1 was related with the aggressive phenotypes of HCC. Functionally, downregulation of HOXD-AS1 repressed the proliferation, invasion abilities of HCC cell in vitro and the distant metastasis of HCC cell in vivo. Further investigations demonstrated that HOXD-AS1 directly bound with miR-326 and thereby regulated its endogenous target gene, solute carrier family 27 member 4 (SLC27A4). CONCLUSIONS: All these findings indicated that HOXD-AS1-miR-326-SLC27A4 axis participated into the progression of HCC.
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spelling pubmed-72164912020-05-18 LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4 Ji, Wenbin Wang, Qunfeng Yang, Jian Cancer Cell Int Primary Research BACKGROUND: Mounting evidences have indicated that long non-coding RNA (lncRNA) HOXD cluster antisense RNA 1 (HOXD-AS1) is dysregulated and participates into the progression of cancers. This study aims to investigate the biological roles and mechanisms of HOXD-AS1 in the metastasis of hepatocellular carcinoma (HCC). METHODS: The quantitative real-time PCR (qPCR) assay was used to assess the level of miR-326 and HOXD-AS1 in HCC tissues and cell lines. The growth of HCC cell was analyzed by using CCK-8 assay and colony formation assay. The migration and invasion of HCC cell were investigated by using wound healing and transwell invasion analysis. The expressions of SLC27A4, N-cadherin and E-cadherin were determined by western blotting. The growth of HCC cell in vivo was assessed by using xenograft model. RESULTS: Here, we elaborated that HOXD-AS1 was overexpressed in HCC tissues than that in the adjacent normal tissues and the level of HOXD-AS1 was related with the aggressive phenotypes of HCC. Functionally, downregulation of HOXD-AS1 repressed the proliferation, invasion abilities of HCC cell in vitro and the distant metastasis of HCC cell in vivo. Further investigations demonstrated that HOXD-AS1 directly bound with miR-326 and thereby regulated its endogenous target gene, solute carrier family 27 member 4 (SLC27A4). CONCLUSIONS: All these findings indicated that HOXD-AS1-miR-326-SLC27A4 axis participated into the progression of HCC. BioMed Central 2020-05-12 /pmc/articles/PMC7216491/ /pubmed/32425696 http://dx.doi.org/10.1186/s12935-020-01217-8 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Primary Research
Ji, Wenbin
Wang, Qunfeng
Yang, Jian
LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title_full LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title_fullStr LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title_full_unstemmed LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title_short LncRNA HOXD-AS1 promotes the metastasis of human hepatocellular carcinoma via modulating miR-326/SLC27A4
title_sort lncrna hoxd-as1 promotes the metastasis of human hepatocellular carcinoma via modulating mir-326/slc27a4
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216491/
https://www.ncbi.nlm.nih.gov/pubmed/32425696
http://dx.doi.org/10.1186/s12935-020-01217-8
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