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miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A

One of the most frequent malignancies in the head and neck is nasopharyngeal carcinoma (NPC). MicroRNAs, a kind of tiny noncoding RNA molecule, have been used as negative regulators in different types of cancer therapy in recent decades by downregulating their targets. Recent research suggests that...

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Autores principales: Lu, Han-qiang, Wang, Run-kun, Wang, Hui-rong, Zhou, Guang-quan, Zhang, Yan-shu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709779/
https://www.ncbi.nlm.nih.gov/pubmed/34956364
http://dx.doi.org/10.1155/2021/6060762
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author Lu, Han-qiang
Wang, Run-kun
Wang, Hui-rong
Zhou, Guang-quan
Zhang, Yan-shu
author_facet Lu, Han-qiang
Wang, Run-kun
Wang, Hui-rong
Zhou, Guang-quan
Zhang, Yan-shu
author_sort Lu, Han-qiang
collection PubMed
description One of the most frequent malignancies in the head and neck is nasopharyngeal carcinoma (NPC). MicroRNAs, a kind of tiny noncoding RNA molecule, have been used as negative regulators in different types of cancer therapy in recent decades by downregulating their targets. Recent research suggests that microRNAs play an important role in cancer's epithelial-to-mesenchymal transition (EMT), supporting or inhibiting EMT development. The epithelial-to-mesenchymal transition (EMT) is linked to a variety of cancer-related activities, including growth, metastasis, and invasion. Previous research has linked EMT to cancer stem-like characteristics as well as treatment resistance. Moreover, since microRNAs (miRNAs) are important regulators of the EMT phenotype, certain miRNAs have an effect on cancer stemness and treatment resistance. As a result, both fundamental research and clinical therapy benefit from knowing the connection between EMT-associated miRNAs and cancer stemness/drug resistance. As a result, we looked at the different functions that EMT-associated miRNAs (miR-137) play in the stem-like characteristics of malignant cells in this article. Then we looked at how EMT-associated miRNAs interact with nasopharyngeal cancer's drug-resistant complex signaling pathways. Using qRT-PCR, we evaluated the performance of several micro RNAs with the proposed miR-137 for inhibiting invasion, metastasis, and the EMT process. In conclusion, our findings showed that miR-137 acted as a tumor suppressor gene in controlling NPC EMT and metastasis and that it may be a new therapeutic strategy and prognosis marker for the disease.
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spelling pubmed-87097792021-12-25 miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A Lu, Han-qiang Wang, Run-kun Wang, Hui-rong Zhou, Guang-quan Zhang, Yan-shu J Oncol Research Article One of the most frequent malignancies in the head and neck is nasopharyngeal carcinoma (NPC). MicroRNAs, a kind of tiny noncoding RNA molecule, have been used as negative regulators in different types of cancer therapy in recent decades by downregulating their targets. Recent research suggests that microRNAs play an important role in cancer's epithelial-to-mesenchymal transition (EMT), supporting or inhibiting EMT development. The epithelial-to-mesenchymal transition (EMT) is linked to a variety of cancer-related activities, including growth, metastasis, and invasion. Previous research has linked EMT to cancer stem-like characteristics as well as treatment resistance. Moreover, since microRNAs (miRNAs) are important regulators of the EMT phenotype, certain miRNAs have an effect on cancer stemness and treatment resistance. As a result, both fundamental research and clinical therapy benefit from knowing the connection between EMT-associated miRNAs and cancer stemness/drug resistance. As a result, we looked at the different functions that EMT-associated miRNAs (miR-137) play in the stem-like characteristics of malignant cells in this article. Then we looked at how EMT-associated miRNAs interact with nasopharyngeal cancer's drug-resistant complex signaling pathways. Using qRT-PCR, we evaluated the performance of several micro RNAs with the proposed miR-137 for inhibiting invasion, metastasis, and the EMT process. In conclusion, our findings showed that miR-137 acted as a tumor suppressor gene in controlling NPC EMT and metastasis and that it may be a new therapeutic strategy and prognosis marker for the disease. Hindawi 2021-12-17 /pmc/articles/PMC8709779/ /pubmed/34956364 http://dx.doi.org/10.1155/2021/6060762 Text en Copyright © 2021 Han-qiang Lu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Lu, Han-qiang
Wang, Run-kun
Wang, Hui-rong
Zhou, Guang-quan
Zhang, Yan-shu
miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title_full miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title_fullStr miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title_full_unstemmed miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title_short miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A
title_sort mir-137 inhibition of the invasion, metastasis, and epithelial-mesenchymal transition of nasopharyngeal cancer by regulating kdm1a
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709779/
https://www.ncbi.nlm.nih.gov/pubmed/34956364
http://dx.doi.org/10.1155/2021/6060762
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