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miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer
OBJECTIVES: It has been accounted that miR‐664a‐3p has different functions in several malignancies; however, the precise role and underlying mechanism in gastric cancer have not been elucidated. Our study aims to explore the function of miR‐664a‐3p on the progression of gastric cancer (GC). METHODS:...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536452/ https://www.ncbi.nlm.nih.gov/pubmed/30883979 http://dx.doi.org/10.1111/cpr.12567 |
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author | Wang, Lu Li, Bowen Zhang, Lu Li, Qing He, Zhongyuan Zhang, Xuan Huang, Xiaoxu Xu, Zhipeng Xia, Yiwen Zhang, Qiang Li, Qiang Xu, Jianghao Sun, Guangli Xu, Zekuan |
author_facet | Wang, Lu Li, Bowen Zhang, Lu Li, Qing He, Zhongyuan Zhang, Xuan Huang, Xiaoxu Xu, Zhipeng Xia, Yiwen Zhang, Qiang Li, Qiang Xu, Jianghao Sun, Guangli Xu, Zekuan |
author_sort | Wang, Lu |
collection | PubMed |
description | OBJECTIVES: It has been accounted that miR‐664a‐3p has different functions in several malignancies; however, the precise role and underlying mechanism in gastric cancer have not been elucidated. Our study aims to explore the function of miR‐664a‐3p on the progression of gastric cancer (GC). METHODS: qRT‐PCR was applied to detect the expression of miR‐664a‐3p in GC tissues and cells. The functions of miR‐664a‐3p on GC in vitro were examined by cell proliferation assay, and transwell assay. Related proteins of epithelial‐mesenchymal transition (EMT) and signal pathway were evaluated by Western blot and immunofluorescence analysis. The bioinformatic, dual‐luciferase assay or ChIP assay were employed to identify the interaction between miR‐664a‐3p and its target gene or Foxp3. The effects in vivo were investigated through a mouse tumorigenicity model. RESULTS: miR‐664a‐3p was frequently upregulated in GC tissues and cells. Elevated expression of miR‐664a‐3p significantly promoted proliferation and invasion in vitro and in vivo. MOB1A was confirmed to be a target of miR‐664a‐3p and restoration of MOB1A attenuated the effects of miR‐664a‐3p. A series of investigations indicated that miR‐664a‐3p contributed to EMT process and inactivated the Hippo pathway by downregulating MOB1A. CONCLUSION: Taken together, we revealed that miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer. |
format | Online Article Text |
id | pubmed-6536452 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-65364522020-03-13 miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer Wang, Lu Li, Bowen Zhang, Lu Li, Qing He, Zhongyuan Zhang, Xuan Huang, Xiaoxu Xu, Zhipeng Xia, Yiwen Zhang, Qiang Li, Qiang Xu, Jianghao Sun, Guangli Xu, Zekuan Cell Prolif Original Articles OBJECTIVES: It has been accounted that miR‐664a‐3p has different functions in several malignancies; however, the precise role and underlying mechanism in gastric cancer have not been elucidated. Our study aims to explore the function of miR‐664a‐3p on the progression of gastric cancer (GC). METHODS: qRT‐PCR was applied to detect the expression of miR‐664a‐3p in GC tissues and cells. The functions of miR‐664a‐3p on GC in vitro were examined by cell proliferation assay, and transwell assay. Related proteins of epithelial‐mesenchymal transition (EMT) and signal pathway were evaluated by Western blot and immunofluorescence analysis. The bioinformatic, dual‐luciferase assay or ChIP assay were employed to identify the interaction between miR‐664a‐3p and its target gene or Foxp3. The effects in vivo were investigated through a mouse tumorigenicity model. RESULTS: miR‐664a‐3p was frequently upregulated in GC tissues and cells. Elevated expression of miR‐664a‐3p significantly promoted proliferation and invasion in vitro and in vivo. MOB1A was confirmed to be a target of miR‐664a‐3p and restoration of MOB1A attenuated the effects of miR‐664a‐3p. A series of investigations indicated that miR‐664a‐3p contributed to EMT process and inactivated the Hippo pathway by downregulating MOB1A. CONCLUSION: Taken together, we revealed that miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer. John Wiley and Sons Inc. 2019-03-18 /pmc/articles/PMC6536452/ /pubmed/30883979 http://dx.doi.org/10.1111/cpr.12567 Text en © 2019 The Authors. Cell Proliferation 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 | Original Articles Wang, Lu Li, Bowen Zhang, Lu Li, Qing He, Zhongyuan Zhang, Xuan Huang, Xiaoxu Xu, Zhipeng Xia, Yiwen Zhang, Qiang Li, Qiang Xu, Jianghao Sun, Guangli Xu, Zekuan miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title | miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title_full | miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title_fullStr | miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title_full_unstemmed | miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title_short | miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer |
title_sort | mir‐664a‐3p functions as an oncogene by targeting hippo pathway in the development of gastric cancer |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536452/ https://www.ncbi.nlm.nih.gov/pubmed/30883979 http://dx.doi.org/10.1111/cpr.12567 |
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