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Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis

Breast cancer (BC) is the most commonly occurring malignancy in women. This study aimed to investigate the functions of the long noncoding RNA ZBED3‐AS1 (ZBED3‐AS1) in BC and its molecular mechanisms. qRT‐PCR was conducted to access the expression of ZBED3‐AS1, microRNA‐513a‐5p (miR‐513a‐5p), and Kr...

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Detalles Bibliográficos
Autores principales: Fu, Aiqin, Yu, Ze, Zhang, Enning, Song, Jijie
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/PMC8520814/
https://www.ncbi.nlm.nih.gov/pubmed/34427978
http://dx.doi.org/10.1111/1759-7714.14111
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author Fu, Aiqin
Yu, Ze
Zhang, Enning
Song, Jijie
author_facet Fu, Aiqin
Yu, Ze
Zhang, Enning
Song, Jijie
author_sort Fu, Aiqin
collection PubMed
description Breast cancer (BC) is the most commonly occurring malignancy in women. This study aimed to investigate the functions of the long noncoding RNA ZBED3‐AS1 (ZBED3‐AS1) in BC and its molecular mechanisms. qRT‐PCR was conducted to access the expression of ZBED3‐AS1, microRNA‐513a‐5p (miR‐513a‐5p), and Kruppel like factor 6 (KLF6) in BC. Additionally, BC cell viability and proliferative capacity were measured by MTT and 5‐Ethynyl‐20‐deoxyuridine (EdU) assays. A transwell assay was used for evaluating BC cell migration and invasion. The interactions among ZBED3‐AS1, miR‐513a‐5p, and KLF6 in BC were confirmed by dual‐luciferase reporter assay. Furthermore, feedback approaches were performed to determine whether ZBED3‐AS1 influences BC cell behaviors by regulating the miR‐513a‐5p/KLF6 axis. The murine xenograft model was established to assess the effect of ZBED3‐AS1 on tumor growth. The expression of ZBED3‐AS1 and KLF6 was reduced, while miR‐513a‐5p expression was elevated in BC. ZBED3‐AS1 elevation attenuated the malignant behaviors of BC cells, including viability, proliferative capacity, migration, and invasion. Mechanical experiments revealed that ZBED3‐AS1 targeted miR‐513a‐5p, and miR‐513a‐5p targeted KLF6 in BC. Feedback approaches validated that miR‐513a‐5p overexpression or KLF6 depletion reversed the inhibitory effects of ZBED3‐AS1 upregulation on viability, proliferative capacity, migration, and invasion of BC cells. Furthermore, ZBED3‐AS1 elevation attenuated the tumor growth in the murine xenograft model. ZBED3‐AS1 hindered the malignant development of BC cells by regulating the miR‐513a‐5p/KLF6 axis, providing a novel therapeutic target in BC.
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spelling pubmed-85208142021-10-25 Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis Fu, Aiqin Yu, Ze Zhang, Enning Song, Jijie Thorac Cancer Original Articles Breast cancer (BC) is the most commonly occurring malignancy in women. This study aimed to investigate the functions of the long noncoding RNA ZBED3‐AS1 (ZBED3‐AS1) in BC and its molecular mechanisms. qRT‐PCR was conducted to access the expression of ZBED3‐AS1, microRNA‐513a‐5p (miR‐513a‐5p), and Kruppel like factor 6 (KLF6) in BC. Additionally, BC cell viability and proliferative capacity were measured by MTT and 5‐Ethynyl‐20‐deoxyuridine (EdU) assays. A transwell assay was used for evaluating BC cell migration and invasion. The interactions among ZBED3‐AS1, miR‐513a‐5p, and KLF6 in BC were confirmed by dual‐luciferase reporter assay. Furthermore, feedback approaches were performed to determine whether ZBED3‐AS1 influences BC cell behaviors by regulating the miR‐513a‐5p/KLF6 axis. The murine xenograft model was established to assess the effect of ZBED3‐AS1 on tumor growth. The expression of ZBED3‐AS1 and KLF6 was reduced, while miR‐513a‐5p expression was elevated in BC. ZBED3‐AS1 elevation attenuated the malignant behaviors of BC cells, including viability, proliferative capacity, migration, and invasion. Mechanical experiments revealed that ZBED3‐AS1 targeted miR‐513a‐5p, and miR‐513a‐5p targeted KLF6 in BC. Feedback approaches validated that miR‐513a‐5p overexpression or KLF6 depletion reversed the inhibitory effects of ZBED3‐AS1 upregulation on viability, proliferative capacity, migration, and invasion of BC cells. Furthermore, ZBED3‐AS1 elevation attenuated the tumor growth in the murine xenograft model. ZBED3‐AS1 hindered the malignant development of BC cells by regulating the miR‐513a‐5p/KLF6 axis, providing a novel therapeutic target in BC. John Wiley & Sons Australia, Ltd 2021-08-24 2021-10 /pmc/articles/PMC8520814/ /pubmed/34427978 http://dx.doi.org/10.1111/1759-7714.14111 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
Fu, Aiqin
Yu, Ze
Zhang, Enning
Song, Jijie
Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title_full Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title_fullStr Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title_full_unstemmed Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title_short Long noncoding RNA ZBED3‐AS1 restrains breast cancer progression by targeting the microRNA‐513a‐5p/KLF6 axis
title_sort long noncoding rna zbed3‐as1 restrains breast cancer progression by targeting the microrna‐513a‐5p/klf6 axis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8520814/
https://www.ncbi.nlm.nih.gov/pubmed/34427978
http://dx.doi.org/10.1111/1759-7714.14111
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