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miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer

BACKGROUND: Breast cancer is the most common malignant tumor diagnosed in women. It is the second leading cause of cancer‐related death among women in the world. Aberrant expression of microRNAs (miRNAs) have been identified to be involved in the development and progression of breast cancer. The aim...

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Autores principales: Wang, Yuli, Shi, Shuang, Wang, Yunshan, Zhang, Xuhua, Liu, Xiaoyan, Li, Juan, Li, Peilong, Du, Lutao, Wang, Chuanxin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8807253/
https://www.ncbi.nlm.nih.gov/pubmed/34953047
http://dx.doi.org/10.1111/1759-7714.14284
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author Wang, Yuli
Shi, Shuang
Wang, Yunshan
Zhang, Xuhua
Liu, Xiaoyan
Li, Juan
Li, Peilong
Du, Lutao
Wang, Chuanxin
author_facet Wang, Yuli
Shi, Shuang
Wang, Yunshan
Zhang, Xuhua
Liu, Xiaoyan
Li, Juan
Li, Peilong
Du, Lutao
Wang, Chuanxin
author_sort Wang, Yuli
collection PubMed
description BACKGROUND: Breast cancer is the most common malignant tumor diagnosed in women. It is the second leading cause of cancer‐related death among women in the world. Aberrant expression of microRNAs (miRNAs) have been identified to be involved in the development and progression of breast cancer. The aim of this study was to investigate the function of miR‐223‐3p in breast cancer progression and metastasis. METHODS: qRT‐PCR was used to analyze the expression levels of miR‐223‐3p in breast cancer tissues and cell lines. Wound healing and Matrigel assays were used to examine cell motility and invasiveness. FBXW7 3′‐UTR construct and luciferase reporter assays were performed for the target gene. RESULTS: miR‐223‐3p was overexpressed in breast cancer tissue and cell lines. A high level of miR‐223‐3p was associated with poor prognosis in breast cancer patients. In addition, overexpressed miR‐223‐3p promoted the migration and invasion of breast cancer cells in vitro and in vivo. Mechanistically, we found that tumor suppressor gene FBXW7 is a target of miR‐223‐3p. Luciferase activity reporter assay indicated miR‐223‐3p could directly bind with the 3′‐UTR of FBXW7. miR‐223‐3p exhibited its oncogenic role partly by decreasing FBXW7 expression, and consequently promoted the invasion and metastasis of breast cancer cells. CONCLUSIONS: Our study revealed a physical and functional relationship among miR‐223‐3p and FBXW7. By negatively regulating FBXW7 expression, miR‐223‐3p exerts a tumor promotion role promoting cell invasion and metastasis in breast cancer.
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spelling pubmed-88072532022-02-04 miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer Wang, Yuli Shi, Shuang Wang, Yunshan Zhang, Xuhua Liu, Xiaoyan Li, Juan Li, Peilong Du, Lutao Wang, Chuanxin Thorac Cancer Original Articles BACKGROUND: Breast cancer is the most common malignant tumor diagnosed in women. It is the second leading cause of cancer‐related death among women in the world. Aberrant expression of microRNAs (miRNAs) have been identified to be involved in the development and progression of breast cancer. The aim of this study was to investigate the function of miR‐223‐3p in breast cancer progression and metastasis. METHODS: qRT‐PCR was used to analyze the expression levels of miR‐223‐3p in breast cancer tissues and cell lines. Wound healing and Matrigel assays were used to examine cell motility and invasiveness. FBXW7 3′‐UTR construct and luciferase reporter assays were performed for the target gene. RESULTS: miR‐223‐3p was overexpressed in breast cancer tissue and cell lines. A high level of miR‐223‐3p was associated with poor prognosis in breast cancer patients. In addition, overexpressed miR‐223‐3p promoted the migration and invasion of breast cancer cells in vitro and in vivo. Mechanistically, we found that tumor suppressor gene FBXW7 is a target of miR‐223‐3p. Luciferase activity reporter assay indicated miR‐223‐3p could directly bind with the 3′‐UTR of FBXW7. miR‐223‐3p exhibited its oncogenic role partly by decreasing FBXW7 expression, and consequently promoted the invasion and metastasis of breast cancer cells. CONCLUSIONS: Our study revealed a physical and functional relationship among miR‐223‐3p and FBXW7. By negatively regulating FBXW7 expression, miR‐223‐3p exerts a tumor promotion role promoting cell invasion and metastasis in breast cancer. John Wiley & Sons Australia, Ltd 2021-12-24 2022-02 /pmc/articles/PMC8807253/ /pubmed/34953047 http://dx.doi.org/10.1111/1759-7714.14284 Text en © 2021 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Wang, Yuli
Shi, Shuang
Wang, Yunshan
Zhang, Xuhua
Liu, Xiaoyan
Li, Juan
Li, Peilong
Du, Lutao
Wang, Chuanxin
miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title_full miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title_fullStr miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title_full_unstemmed miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title_short miR‐223‐3p targets FBXW7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
title_sort mir‐223‐3p targets fbxw7 to promote epithelial‐mesenchymal transition and metastasis in breast cancer
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8807253/
https://www.ncbi.nlm.nih.gov/pubmed/34953047
http://dx.doi.org/10.1111/1759-7714.14284
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