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Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2
BACKGROUND: Keloids are benign fibroproliferative skin tumors. Circular RNA (circRNA) hsa_circ_0043688 has been exhibited to the freakishly expressed in keloid tissues. Here, we aimed to investigate the regulatory network of hsa_circ_0043688 in the pathological process of keloid. METHODS: Hsa_circ_0...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9396203/ https://www.ncbi.nlm.nih.gov/pubmed/35754140 http://dx.doi.org/10.1002/jcla.24528 |
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author | Liu, Ye Wang, Xin Ni, Ziqiao Li, Yinqiu Song, Jiaqian Zhu, Fei li, Xiaojing |
author_facet | Liu, Ye Wang, Xin Ni, Ziqiao Li, Yinqiu Song, Jiaqian Zhu, Fei li, Xiaojing |
author_sort | Liu, Ye |
collection | PubMed |
description | BACKGROUND: Keloids are benign fibroproliferative skin tumors. Circular RNA (circRNA) hsa_circ_0043688 has been exhibited to the freakishly expressed in keloid tissues. Here, we aimed to investigate the regulatory network of hsa_circ_0043688 in the pathological process of keloid. METHODS: Hsa_circ_0043688, microRNA‐145‐5p (miR‐145‐5p), and Fibroblast growth factor‐2 (FGF2) level were detected using RT‐qPCR. Cell viability, proliferation, apoptosis, invasion, and migration were investigated using Cell Counting Kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, transwell, and wound healing assays, respectively. Western blot analysis of protein levels of FGF2, CyclinD1, Collagen I, and Collagen III. After the prediction of Circinteractome and Starbase, their interaction was verified based on a dual‐luciferase reporter and RIP assays. RESULTS: Increased hsa_circ_0043688 and FGF2, and decreased miR‐145‐5p in keloids samples and fibroblasts were found. Also, hsa_circ_0043688 absence hindered proliferation, invasion, migration, and boost apoptosis of keloid fibroblasts. In mechanism, hsa_circ_0043688 modulated FGF2 content via sponging miR‐145‐5p. CONCLUSION: Hsa_circ_0043688 knockdown inhibited cell growth and metastasis of keloid fibroblasts via miR‐145‐5p/FGF2, providing a new mechanism to understand the keloid progression. |
format | Online Article Text |
id | pubmed-9396203 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93962032022-08-24 Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 Liu, Ye Wang, Xin Ni, Ziqiao Li, Yinqiu Song, Jiaqian Zhu, Fei li, Xiaojing J Clin Lab Anal Research Articles BACKGROUND: Keloids are benign fibroproliferative skin tumors. Circular RNA (circRNA) hsa_circ_0043688 has been exhibited to the freakishly expressed in keloid tissues. Here, we aimed to investigate the regulatory network of hsa_circ_0043688 in the pathological process of keloid. METHODS: Hsa_circ_0043688, microRNA‐145‐5p (miR‐145‐5p), and Fibroblast growth factor‐2 (FGF2) level were detected using RT‐qPCR. Cell viability, proliferation, apoptosis, invasion, and migration were investigated using Cell Counting Kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, transwell, and wound healing assays, respectively. Western blot analysis of protein levels of FGF2, CyclinD1, Collagen I, and Collagen III. After the prediction of Circinteractome and Starbase, their interaction was verified based on a dual‐luciferase reporter and RIP assays. RESULTS: Increased hsa_circ_0043688 and FGF2, and decreased miR‐145‐5p in keloids samples and fibroblasts were found. Also, hsa_circ_0043688 absence hindered proliferation, invasion, migration, and boost apoptosis of keloid fibroblasts. In mechanism, hsa_circ_0043688 modulated FGF2 content via sponging miR‐145‐5p. CONCLUSION: Hsa_circ_0043688 knockdown inhibited cell growth and metastasis of keloid fibroblasts via miR‐145‐5p/FGF2, providing a new mechanism to understand the keloid progression. John Wiley and Sons Inc. 2022-06-26 /pmc/articles/PMC9396203/ /pubmed/35754140 http://dx.doi.org/10.1002/jcla.24528 Text en © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. 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 | Research Articles Liu, Ye Wang, Xin Ni, Ziqiao Li, Yinqiu Song, Jiaqian Zhu, Fei li, Xiaojing Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title | Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title_full | Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title_fullStr | Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title_full_unstemmed | Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title_short | Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA‐145‐5p to promote the progression of Keloids via Fibroblast growth factor‐2 |
title_sort | circular rna hsa_circ_0043688 serves as a competing endogenous rna for microrna‐145‐5p to promote the progression of keloids via fibroblast growth factor‐2 |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9396203/ https://www.ncbi.nlm.nih.gov/pubmed/35754140 http://dx.doi.org/10.1002/jcla.24528 |
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