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lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway

Increasing evidence has indicated the important roles of long noncoding RNA small nucleolar RNA host gene 7 (SNHG7) in tumourigenesis as a potential oncogene. However, the function of SNHG7 in hepatic carcinoma remains unclear. In the present study, we found that SNHG7 expression was significantly u...

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Autores principales: Yao, Xuebing, Liu, Chi, Liu, Cuiyun, Xi, Wenna, Sun, Shuilin, Gao, Zhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851833/
https://www.ncbi.nlm.nih.gov/pubmed/31478234
http://dx.doi.org/10.1002/cbf.3429
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author Yao, Xuebing
Liu, Chi
Liu, Cuiyun
Xi, Wenna
Sun, Shuilin
Gao, Zhen
author_facet Yao, Xuebing
Liu, Chi
Liu, Cuiyun
Xi, Wenna
Sun, Shuilin
Gao, Zhen
author_sort Yao, Xuebing
collection PubMed
description Increasing evidence has indicated the important roles of long noncoding RNA small nucleolar RNA host gene 7 (SNHG7) in tumourigenesis as a potential oncogene. However, the function of SNHG7 in hepatic carcinoma remains unclear. In the present study, we found that SNHG7 expression was significantly upregulated in hepatic carcinoma tissues, especially in aggressive cases, and it was closely correlated with the poor prognosis. Furthermore, knockdown of SNHG7 inhibited the proliferation, migration, and invasion of hepatic carcinoma cell lines in vitro. Mechanistically, SNHG7 directly interacted with miR‐425 as a ceRNA. Moreover, knockdown of SNHG7 significantly inhibited the tumorigenic Wnt/β‐catenin/EMT pathway. SNHG7 regulated Wnt/β‐catenin/EMT pathway through sponging miR‐425 and played an oncogenic role in hepatic carcinoma progression. Together, our study elucidated the role of SNHG7 as a ceRNA in hepatic carcinoma, provided new potential diagnosis and therapeutic application in hepatic carcinoma progression. SIGNIFICANCE OF THE STUDY: SNHG7 could promote proliferation and metastasis of hepatic carcinoma cell in vitro and in vivo, suggesting that SNHG7 exerts tumorigenic role in hepatic carcinoma progression. Further mechanism research revealed that SNHG7 exhibited the tumorigenic role through Wnt/β‐catenin/EMT pathway as a miR‐425 sponge. These findings provided new cues to understand the molecular signalling network in carcinogenesis of hepatic carcinoma, and it may provide new evidence for therapeutic application in hepatic carcinoma.
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spelling pubmed-68518332019-11-18 lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway Yao, Xuebing Liu, Chi Liu, Cuiyun Xi, Wenna Sun, Shuilin Gao, Zhen Cell Biochem Funct Research Articles Increasing evidence has indicated the important roles of long noncoding RNA small nucleolar RNA host gene 7 (SNHG7) in tumourigenesis as a potential oncogene. However, the function of SNHG7 in hepatic carcinoma remains unclear. In the present study, we found that SNHG7 expression was significantly upregulated in hepatic carcinoma tissues, especially in aggressive cases, and it was closely correlated with the poor prognosis. Furthermore, knockdown of SNHG7 inhibited the proliferation, migration, and invasion of hepatic carcinoma cell lines in vitro. Mechanistically, SNHG7 directly interacted with miR‐425 as a ceRNA. Moreover, knockdown of SNHG7 significantly inhibited the tumorigenic Wnt/β‐catenin/EMT pathway. SNHG7 regulated Wnt/β‐catenin/EMT pathway through sponging miR‐425 and played an oncogenic role in hepatic carcinoma progression. Together, our study elucidated the role of SNHG7 as a ceRNA in hepatic carcinoma, provided new potential diagnosis and therapeutic application in hepatic carcinoma progression. SIGNIFICANCE OF THE STUDY: SNHG7 could promote proliferation and metastasis of hepatic carcinoma cell in vitro and in vivo, suggesting that SNHG7 exerts tumorigenic role in hepatic carcinoma progression. Further mechanism research revealed that SNHG7 exhibited the tumorigenic role through Wnt/β‐catenin/EMT pathway as a miR‐425 sponge. These findings provided new cues to understand the molecular signalling network in carcinogenesis of hepatic carcinoma, and it may provide new evidence for therapeutic application in hepatic carcinoma. John Wiley and Sons Inc. 2019-09-02 2019-10 /pmc/articles/PMC6851833/ /pubmed/31478234 http://dx.doi.org/10.1002/cbf.3429 Text en © 2019 The Authors. Cell Biochemistry and Function Published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Yao, Xuebing
Liu, Chi
Liu, Cuiyun
Xi, Wenna
Sun, Shuilin
Gao, Zhen
lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title_full lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title_fullStr lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title_full_unstemmed lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title_short lncRNA SNHG7 sponges miR‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via Wnt/β‐catenin/EMT signalling pathway
title_sort lncrna snhg7 sponges mir‐425 to promote proliferation, migration, and invasion of hepatic carcinoma cells via wnt/β‐catenin/emt signalling pathway
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851833/
https://www.ncbi.nlm.nih.gov/pubmed/31478234
http://dx.doi.org/10.1002/cbf.3429
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