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Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer

BACKGROUND: Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. METHODS: RT‐PCR was used to detect HCG18 and miR‐141‐3p e...

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Detalles Bibliográficos
Autores principales: Liu, Yan, Lin, Wenji, Dong, Yangyang, Li, Xinyu, Lin, Zhibin, Jia, Jing, Zou, Wenbing, Pan, Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520348/
https://www.ncbi.nlm.nih.gov/pubmed/32725768
http://dx.doi.org/10.1002/cam4.3288
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author Liu, Yan
Lin, Wenji
Dong, Yangyang
Li, Xinyu
Lin, Zhibin
Jia, Jing
Zou, Wenbing
Pan, Yu
author_facet Liu, Yan
Lin, Wenji
Dong, Yangyang
Li, Xinyu
Lin, Zhibin
Jia, Jing
Zou, Wenbing
Pan, Yu
author_sort Liu, Yan
collection PubMed
description BACKGROUND: Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. METHODS: RT‐PCR was used to detect HCG18 and miR‐141‐3p expression in GC specimen. GC cell lines (AGS and MKN‐28) were exploited as cell model. The biological effect of HCG18 on cancer cells was probed by CCK‐8, colony formation, flow cytometry, Transwell and wound‐healing experiments in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Interaction between HCG18 and miR‐141‐3p was determined by bioinformatics analysis, RT‐PCR, and luciferase reporter experiments. Downstream gene expression of miR‐141‐3p, including Wiskott–Aldrich syndrome protein interacting protein family member 1 (WIPF1), Yes associated protein 1 (YAP), and tafazzin (TAZ) were detected using Western blot. RESULTS: HCG18 was markedly up‐regulated in GC specimens, while miR‐141‐3p was markedly down‐regulated. Down‐regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR‐141‐3p transfection led to opposite effect. HCG18 could down‐regulate miR‐141‐3p through adsorbing it, and a negative association between HCG18 and miR‐141‐3p was found in GC specimens. HCG18 promoted WIPF1, YAP and TAZ expression, nonetheless, such influence was reversed by co‐transfecting with miR‐141‐3p. CONCLUSION: HCG18 was aberrantly up‐regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR‐141‐3p expression.
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spelling pubmed-75203482020-09-30 Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer Liu, Yan Lin, Wenji Dong, Yangyang Li, Xinyu Lin, Zhibin Jia, Jing Zou, Wenbing Pan, Yu Cancer Med Cancer Biology BACKGROUND: Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. METHODS: RT‐PCR was used to detect HCG18 and miR‐141‐3p expression in GC specimen. GC cell lines (AGS and MKN‐28) were exploited as cell model. The biological effect of HCG18 on cancer cells was probed by CCK‐8, colony formation, flow cytometry, Transwell and wound‐healing experiments in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Interaction between HCG18 and miR‐141‐3p was determined by bioinformatics analysis, RT‐PCR, and luciferase reporter experiments. Downstream gene expression of miR‐141‐3p, including Wiskott–Aldrich syndrome protein interacting protein family member 1 (WIPF1), Yes associated protein 1 (YAP), and tafazzin (TAZ) were detected using Western blot. RESULTS: HCG18 was markedly up‐regulated in GC specimens, while miR‐141‐3p was markedly down‐regulated. Down‐regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR‐141‐3p transfection led to opposite effect. HCG18 could down‐regulate miR‐141‐3p through adsorbing it, and a negative association between HCG18 and miR‐141‐3p was found in GC specimens. HCG18 promoted WIPF1, YAP and TAZ expression, nonetheless, such influence was reversed by co‐transfecting with miR‐141‐3p. CONCLUSION: HCG18 was aberrantly up‐regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR‐141‐3p expression. John Wiley and Sons Inc. 2020-07-29 /pmc/articles/PMC7520348/ /pubmed/32725768 http://dx.doi.org/10.1002/cam4.3288 Text en © 2020 The Authors. Cancer Medicine 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 Cancer Biology
Liu, Yan
Lin, Wenji
Dong, Yangyang
Li, Xinyu
Lin, Zhibin
Jia, Jing
Zou, Wenbing
Pan, Yu
Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title_full Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title_fullStr Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title_full_unstemmed Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title_short Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer
title_sort long noncoding rna hcg18 up‐regulates the expression of wipf1 and yap/taz by inhibiting mir‐141‐3p in gastric cancer
topic Cancer Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520348/
https://www.ncbi.nlm.nih.gov/pubmed/32725768
http://dx.doi.org/10.1002/cam4.3288
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