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MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways
MicroRNAs are beneficial for cancer therapy as they can simultaneously downregulate multiple targets involved in diverse biological pathways related to tumor development. In papillary thyroid cancer, many microRNAs were identified as differentially expressed factors in tumor tissues. In another way,...
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/PMC6618135/ https://www.ncbi.nlm.nih.gov/pubmed/30941771 http://dx.doi.org/10.1002/jcp.28472 |
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author | Liu, Hui Chen, Xi Lin, Ting Chen, Xingsheng Yan, Jiqi Jiang, Shan |
author_facet | Liu, Hui Chen, Xi Lin, Ting Chen, Xingsheng Yan, Jiqi Jiang, Shan |
author_sort | Liu, Hui |
collection | PubMed |
description | MicroRNAs are beneficial for cancer therapy as they can simultaneously downregulate multiple targets involved in diverse biological pathways related to tumor development. In papillary thyroid cancer, many microRNAs were identified as differentially expressed factors in tumor tissues. In another way, recent studies revealed cell proliferation, cell cycling, apoptosis, and autophagy are critical pathways controlling papillary thyroid cancer development and progression. As miR‐524‐5p was approved as a cancer suppressor targeting multiple genes in several types of cancer cells, this study aims to characterize the role of miR‐524‐5p in the thyroid cancer cell. The expression of miR‐524‐5p was decreased in the papillary thyroid cancer tissues and cell lines, while forkhead box E1 (FOXE1) and ITGA3 were increased. In the clinical case, expression of miR‐524‐5p, FOXE1, and ITGA3 were significantly correlated with papillary thyroid cancer development and progression. FOXE1 and ITGA3 were approved as direct targets of miR‐524‐5p. miR‐524‐5p could inhibit papillary thyroid cancer cell viability, migration, invasion, and apoptosis through targeting FOXE1 and ITGA3. Cell cycling and autophagy pathways were disturbed by downregulation of FOXE1 and ITGA3, respectively. Collectively, miR‐524‐5p targeting on FOXE1 and ITGA3 prevents thyroid cancer progression through different pathways including cell cycling and autophagy. |
format | Online Article Text |
id | pubmed-6618135 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-66181352019-07-22 MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways Liu, Hui Chen, Xi Lin, Ting Chen, Xingsheng Yan, Jiqi Jiang, Shan J Cell Physiol Original Research Articles MicroRNAs are beneficial for cancer therapy as they can simultaneously downregulate multiple targets involved in diverse biological pathways related to tumor development. In papillary thyroid cancer, many microRNAs were identified as differentially expressed factors in tumor tissues. In another way, recent studies revealed cell proliferation, cell cycling, apoptosis, and autophagy are critical pathways controlling papillary thyroid cancer development and progression. As miR‐524‐5p was approved as a cancer suppressor targeting multiple genes in several types of cancer cells, this study aims to characterize the role of miR‐524‐5p in the thyroid cancer cell. The expression of miR‐524‐5p was decreased in the papillary thyroid cancer tissues and cell lines, while forkhead box E1 (FOXE1) and ITGA3 were increased. In the clinical case, expression of miR‐524‐5p, FOXE1, and ITGA3 were significantly correlated with papillary thyroid cancer development and progression. FOXE1 and ITGA3 were approved as direct targets of miR‐524‐5p. miR‐524‐5p could inhibit papillary thyroid cancer cell viability, migration, invasion, and apoptosis through targeting FOXE1 and ITGA3. Cell cycling and autophagy pathways were disturbed by downregulation of FOXE1 and ITGA3, respectively. Collectively, miR‐524‐5p targeting on FOXE1 and ITGA3 prevents thyroid cancer progression through different pathways including cell cycling and autophagy. John Wiley and Sons Inc. 2019-04-02 2019-10 /pmc/articles/PMC6618135/ /pubmed/30941771 http://dx.doi.org/10.1002/jcp.28472 Text en © 2019 The Authors Journal of Cellular Physiology Published by Wiley Periodicals, Inc. 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 Research Articles Liu, Hui Chen, Xi Lin, Ting Chen, Xingsheng Yan, Jiqi Jiang, Shan MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title | MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title_full | MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title_fullStr | MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title_full_unstemmed | MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title_short | MicroRNA‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways |
title_sort | microrna‐524‐5p suppresses the progression of papillary thyroid carcinoma cells via targeting on foxe1 and itga3 in cell autophagy and cycling pathways |
topic | Original Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6618135/ https://www.ncbi.nlm.nih.gov/pubmed/30941771 http://dx.doi.org/10.1002/jcp.28472 |
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