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MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy
BACKGROUND: Papillary thyroid carcinoma (PTC) grows slowly but has a great risk of metastasis. MicroRNAs are well known as vital tumor‐related gene regulators. In PTC, the role of miR‐203a‐3p and the underlying mechanisms remain not completely understood. METHODS: We conducted CCK8 assay, wound heal...
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/PMC9169216/ https://www.ncbi.nlm.nih.gov/pubmed/35524422 http://dx.doi.org/10.1002/jcla.24470 |
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author | Dai, Lei Zhang, Weidong Wu, Xianjiang Zhou, Shuihong |
author_facet | Dai, Lei Zhang, Weidong Wu, Xianjiang Zhou, Shuihong |
author_sort | Dai, Lei |
collection | PubMed |
description | BACKGROUND: Papillary thyroid carcinoma (PTC) grows slowly but has a great risk of metastasis. MicroRNAs are well known as vital tumor‐related gene regulators. In PTC, the role of miR‐203a‐3p and the underlying mechanisms remain not completely understood. METHODS: We conducted CCK8 assay, wound healing assay, transwell experiment and flow cytometry analyses to investigate the function of miRNA‐203a‐3p. The interaction of miRNA‐203a‐3p with its gene MAP3K1 was characterized by quantitative real‐time polymerase chain reaction, western blotting and luciferase assay. RESULTS: We found that the levels of miRNA‐203a‐3p were statistically decreased in PTC tissues. When mimics were delivered to TPC‐1 and KTC‐1 cells to upregulate miR‐203a‐3p, it was observed that cell proliferation, metastatic abilities and cell cycle process were prevented but cell apoptosis was enhanced. Furthermore, we proved the interaction between MAP3K1 and miR‐203a‐3p. Intriguingly, similar to miR‐203a‐3p mimics, siMAP3K1 showed a tumor‐suppressive effect, and this effect could be reversed when miR‐203a‐3p was simultaneously inhibited. Finally, selected autophagy‐linked proteins such as LC3 Beclin‐1 were detected and found to be increased when miR‐203a‐3p was upregulated or MAP3K1 was inhibited. CONCLUSION: Overall, miR‐203a‐3p inhibits the oncogenic characteristics of TPC‐1 and KTC‐1 cells via suppressing MAP3K1 and activating autophagy. Our findings might enrich the understanding and the therapeutic strategies of PTC. |
format | Online Article Text |
id | pubmed-9169216 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-91692162022-06-07 MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy Dai, Lei Zhang, Weidong Wu, Xianjiang Zhou, Shuihong J Clin Lab Anal Research Articles BACKGROUND: Papillary thyroid carcinoma (PTC) grows slowly but has a great risk of metastasis. MicroRNAs are well known as vital tumor‐related gene regulators. In PTC, the role of miR‐203a‐3p and the underlying mechanisms remain not completely understood. METHODS: We conducted CCK8 assay, wound healing assay, transwell experiment and flow cytometry analyses to investigate the function of miRNA‐203a‐3p. The interaction of miRNA‐203a‐3p with its gene MAP3K1 was characterized by quantitative real‐time polymerase chain reaction, western blotting and luciferase assay. RESULTS: We found that the levels of miRNA‐203a‐3p were statistically decreased in PTC tissues. When mimics were delivered to TPC‐1 and KTC‐1 cells to upregulate miR‐203a‐3p, it was observed that cell proliferation, metastatic abilities and cell cycle process were prevented but cell apoptosis was enhanced. Furthermore, we proved the interaction between MAP3K1 and miR‐203a‐3p. Intriguingly, similar to miR‐203a‐3p mimics, siMAP3K1 showed a tumor‐suppressive effect, and this effect could be reversed when miR‐203a‐3p was simultaneously inhibited. Finally, selected autophagy‐linked proteins such as LC3 Beclin‐1 were detected and found to be increased when miR‐203a‐3p was upregulated or MAP3K1 was inhibited. CONCLUSION: Overall, miR‐203a‐3p inhibits the oncogenic characteristics of TPC‐1 and KTC‐1 cells via suppressing MAP3K1 and activating autophagy. Our findings might enrich the understanding and the therapeutic strategies of PTC. John Wiley and Sons Inc. 2022-05-06 /pmc/articles/PMC9169216/ /pubmed/35524422 http://dx.doi.org/10.1002/jcla.24470 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 Dai, Lei Zhang, Weidong Wu, Xianjiang Zhou, Shuihong MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title | MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title_full | MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title_fullStr | MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title_full_unstemmed | MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title_short | MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy |
title_sort | microrna‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing map3k1 and activating autophagy |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9169216/ https://www.ncbi.nlm.nih.gov/pubmed/35524422 http://dx.doi.org/10.1002/jcla.24470 |
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