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lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression

BACKGROUND: The long non‐coding RNA HAND2 antisense RNA 1 (HAND2‐AS1) acts as a tumor suppressor in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the function of HAND2‐AS1 in HCC. METHODS: The expression levels of HAND2‐A...

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Autores principales: Jing, Gui‐Ying, Zheng, Xuan‐Zhen, Ji, Xiao‐Xia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8059724/
https://www.ncbi.nlm.nih.gov/pubmed/33566427
http://dx.doi.org/10.1002/jcla.23717
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author Jing, Gui‐Ying
Zheng, Xuan‐Zhen
Ji, Xiao‐Xia
author_facet Jing, Gui‐Ying
Zheng, Xuan‐Zhen
Ji, Xiao‐Xia
author_sort Jing, Gui‐Ying
collection PubMed
description BACKGROUND: The long non‐coding RNA HAND2 antisense RNA 1 (HAND2‐AS1) acts as a tumor suppressor in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the function of HAND2‐AS1 in HCC. METHODS: The expression levels of HAND2‐AS1 and runt‐related transcription factor 2 (RUNX2) were determined in patients with HCC and HCC cell lines using quantitative real‐time polymerase chain reaction and western blot analyses. Cell proliferation was determined using Cell Counting Kit‐8 assay, and the correlation between HAND2‐AS1 and RUNX2 expression was also investigated. RESULTS: The plasma level of HAND2‐AS1 was downregulated and that of RUNX2 was upregulated in patients with early‐stage HCC compared with those in healthy controls. No significant differences in the plasma levels of HAND2‐AS1 and RUNX2 were found among hepatitis B virus (HBV)‐positive, hepatitis C virus (HCV)‐positive, and HBV‐ and HCV‐negative patients with HCC. The plasma levels of HAND2‐AS1 and RUNX2 were inversely correlated in the patient groups but not in the control group. HAND2‐AS1 overexpression led to the downregulation of RUNX2 expression in human HCC cells, whereas RUNX2 failed to significantly affect HAND2‐AS1 expression. HAND2‐AS1 overexpression inhibited and RUNX2 overexpression promoted the proliferation of HCC cells. RUNX2 overexpression attenuated the inhibitory effects of HAND2‐AS1 overexpression on cancer cell proliferation. CONCLUSION: HAND2‐AS1 overexpression inhibits cancer cell proliferation in HCC by downregulating RUNX2 expression.
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spelling pubmed-80597242021-04-23 lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression Jing, Gui‐Ying Zheng, Xuan‐Zhen Ji, Xiao‐Xia J Clin Lab Anal Research Articles BACKGROUND: The long non‐coding RNA HAND2 antisense RNA 1 (HAND2‐AS1) acts as a tumor suppressor in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the function of HAND2‐AS1 in HCC. METHODS: The expression levels of HAND2‐AS1 and runt‐related transcription factor 2 (RUNX2) were determined in patients with HCC and HCC cell lines using quantitative real‐time polymerase chain reaction and western blot analyses. Cell proliferation was determined using Cell Counting Kit‐8 assay, and the correlation between HAND2‐AS1 and RUNX2 expression was also investigated. RESULTS: The plasma level of HAND2‐AS1 was downregulated and that of RUNX2 was upregulated in patients with early‐stage HCC compared with those in healthy controls. No significant differences in the plasma levels of HAND2‐AS1 and RUNX2 were found among hepatitis B virus (HBV)‐positive, hepatitis C virus (HCV)‐positive, and HBV‐ and HCV‐negative patients with HCC. The plasma levels of HAND2‐AS1 and RUNX2 were inversely correlated in the patient groups but not in the control group. HAND2‐AS1 overexpression led to the downregulation of RUNX2 expression in human HCC cells, whereas RUNX2 failed to significantly affect HAND2‐AS1 expression. HAND2‐AS1 overexpression inhibited and RUNX2 overexpression promoted the proliferation of HCC cells. RUNX2 overexpression attenuated the inhibitory effects of HAND2‐AS1 overexpression on cancer cell proliferation. CONCLUSION: HAND2‐AS1 overexpression inhibits cancer cell proliferation in HCC by downregulating RUNX2 expression. John Wiley and Sons Inc. 2021-02-10 /pmc/articles/PMC8059724/ /pubmed/33566427 http://dx.doi.org/10.1002/jcla.23717 Text en © 2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Research Articles
Jing, Gui‐Ying
Zheng, Xuan‐Zhen
Ji, Xiao‐Xia
lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title_full lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title_fullStr lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title_full_unstemmed lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title_short lncRNA HAND2‐AS1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating RUNX2 expression
title_sort lncrna hand2‐as1 overexpression inhibits cancer cell proliferation in hepatocellular carcinoma by downregulating runx2 expression
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8059724/
https://www.ncbi.nlm.nih.gov/pubmed/33566427
http://dx.doi.org/10.1002/jcla.23717
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