DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis

BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to be biological regulators in hepatocellular carcinoma (HCC). DLG1 antisense RNA 1 (DLG1-AS1) has been found to be up-regulated in cervical cancer. However, its function and underlying mechanism in HCC remains unknown. METHODS: DLG1-AS1...

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Autores principales: Min, Jie, Jin, Dayong, Zhang, Feng, Kang, Yanxia, Qi, Yuhong, Du, Pang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Primary Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789637/
https://www.ncbi.nlm.nih.gov/pubmed/33407499
http://dx.doi.org/10.1186/s12935-020-01667-0
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author Min, Jie
Jin, Dayong
Zhang, Feng
Kang, Yanxia
Qi, Yuhong
Du, Pang
author_facet Min, Jie
Jin, Dayong
Zhang, Feng
Kang, Yanxia
Qi, Yuhong
Du, Pang
author_sort Min, Jie
collection PubMed
description BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to be biological regulators in hepatocellular carcinoma (HCC). DLG1 antisense RNA 1 (DLG1-AS1) has been found to be up-regulated in cervical cancer. However, its function and underlying mechanism in HCC remains unknown. METHODS: DLG1-AS1 expression was assessed in HCC cells and normal cell by RT-qPCR. Luciferase reporter assay, RNA pull down assay and RIP assay were used to demonstrate the interaction between DLG1-AS1 and miR-497-5p. RESULTS: DLG1-AS1 was highly expressed in HCC cells. Silencing of DLG1-AS1 led to the inhibition of HCC cell growth and migration. Besides, MYC induced the transcriptional activation of DLG1-AS1. MYC could facilitate HCC cellular processes by up-regulating DLG1-AS1. MiR-497-5p could interact with DLG1-AS1 in HCC cells. Down-regulation of miR-497-5p could reverse the impacts of DLG1-AS1 silencing on HCC cells. SSRP1 expression could be positively regulated by DLG1-AS1 but was negatively regulated by miR-497-5p. Knockdown of DLG1-AS1 suppressed tumor growth in nude mice. CONCLUSIONS: DLG1-AS1 is activated by MYC and functions as an oncogene in HCC via miR-497-5p/SSRP1 axis. [Image: see text]
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spelling pubmed-77896372021-01-07 DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis Min, Jie Jin, Dayong Zhang, Feng Kang, Yanxia Qi, Yuhong Du, Pang Cancer Cell Int Primary Research BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to be biological regulators in hepatocellular carcinoma (HCC). DLG1 antisense RNA 1 (DLG1-AS1) has been found to be up-regulated in cervical cancer. However, its function and underlying mechanism in HCC remains unknown. METHODS: DLG1-AS1 expression was assessed in HCC cells and normal cell by RT-qPCR. Luciferase reporter assay, RNA pull down assay and RIP assay were used to demonstrate the interaction between DLG1-AS1 and miR-497-5p. RESULTS: DLG1-AS1 was highly expressed in HCC cells. Silencing of DLG1-AS1 led to the inhibition of HCC cell growth and migration. Besides, MYC induced the transcriptional activation of DLG1-AS1. MYC could facilitate HCC cellular processes by up-regulating DLG1-AS1. MiR-497-5p could interact with DLG1-AS1 in HCC cells. Down-regulation of miR-497-5p could reverse the impacts of DLG1-AS1 silencing on HCC cells. SSRP1 expression could be positively regulated by DLG1-AS1 but was negatively regulated by miR-497-5p. Knockdown of DLG1-AS1 suppressed tumor growth in nude mice. CONCLUSIONS: DLG1-AS1 is activated by MYC and functions as an oncogene in HCC via miR-497-5p/SSRP1 axis. [Image: see text] BioMed Central 2021-01-06 /pmc/articles/PMC7789637/ /pubmed/33407499 http://dx.doi.org/10.1186/s12935-020-01667-0 Text en © The Author(s) 2021 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
Min, Jie
Jin, Dayong
Zhang, Feng
Kang, Yanxia
Qi, Yuhong
Du, Pang
DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title_full DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title_fullStr DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title_full_unstemmed DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title_short DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis
title_sort dlg1-as1 is activated by myc and drives the proliferation and migration of hepatocellular carcinoma cells through mir-497-5p/ssrp1 axis
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789637/
https://www.ncbi.nlm.nih.gov/pubmed/33407499
http://dx.doi.org/10.1186/s12935-020-01667-0
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