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MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3

Cervical cancer is the third most common gynecological cancer and the fourth leading cause of cancer-related deaths in women around the world. Substantial evidence has demonstrated that microRNA (miRNA) expression is disordered in many malignant tumors. The dysregulation of miRNAs has been suggested...

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Autores principales: Shan, Dan, Shang, Yumin, Hu, Tongxiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848402/
https://www.ncbi.nlm.nih.gov/pubmed/29716674
http://dx.doi.org/10.3727/096504018X15247361080118
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author Shan, Dan
Shang, Yumin
Hu, Tongxiu
author_facet Shan, Dan
Shang, Yumin
Hu, Tongxiu
author_sort Shan, Dan
collection PubMed
description Cervical cancer is the third most common gynecological cancer and the fourth leading cause of cancer-related deaths in women around the world. Substantial evidence has demonstrated that microRNA (miRNA) expression is disordered in many malignant tumors. The dysregulation of miRNAs has been suggested to be involved in the tumorigenesis and tumor development of cervical cancer. Therefore, identification of miRNAs and their biological roles and targets involved in tumor pathology would provide valuable insight into the diagnosis and treatment of patients with cervical cancer. MicroRNA-411 (miR-411) has been reported to play an important role in several types of human cancer. However, the expression level, role, and underlying molecular mechanisms of miR-411 in cervical cancer remain unclear. Therefore, the objectives of this study were to investigate the expression pattern and clinical significance of miR-411 in cervical cancer and to evaluate its role and underlying mechanisms in this disease. In this study, we confirmed that the expression of miR-411 was significantly downregulated in both cervical cancer tissues and cell lines. Low expression of miR-411 was associated with tumor size, FIGO stage, lymph node metastasis, and distant metastasis. Additionally, miR-411 overexpression inhibited cell proliferation and invasion in cervical cancer. Furthermore, signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-411 in this disease. In clinical samples, miR-411 expression levels were inversely correlated with STAT3, which was significantly upregulated in cervical cancer. Restored STAT3 expression abolished the tumor-suppressing effects of miR-411 overexpression on the proliferation and invasion of cervical cancer cells. In conclusion, our data demonstrated that miR-411 inhibited cervical cancer progression by directly targeting STAT3 and may represent a novel potential therapeutic target and prognostic marker for patients with this disease.
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spelling pubmed-78484022021-02-16 MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3 Shan, Dan Shang, Yumin Hu, Tongxiu Oncol Res Article Cervical cancer is the third most common gynecological cancer and the fourth leading cause of cancer-related deaths in women around the world. Substantial evidence has demonstrated that microRNA (miRNA) expression is disordered in many malignant tumors. The dysregulation of miRNAs has been suggested to be involved in the tumorigenesis and tumor development of cervical cancer. Therefore, identification of miRNAs and their biological roles and targets involved in tumor pathology would provide valuable insight into the diagnosis and treatment of patients with cervical cancer. MicroRNA-411 (miR-411) has been reported to play an important role in several types of human cancer. However, the expression level, role, and underlying molecular mechanisms of miR-411 in cervical cancer remain unclear. Therefore, the objectives of this study were to investigate the expression pattern and clinical significance of miR-411 in cervical cancer and to evaluate its role and underlying mechanisms in this disease. In this study, we confirmed that the expression of miR-411 was significantly downregulated in both cervical cancer tissues and cell lines. Low expression of miR-411 was associated with tumor size, FIGO stage, lymph node metastasis, and distant metastasis. Additionally, miR-411 overexpression inhibited cell proliferation and invasion in cervical cancer. Furthermore, signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-411 in this disease. In clinical samples, miR-411 expression levels were inversely correlated with STAT3, which was significantly upregulated in cervical cancer. Restored STAT3 expression abolished the tumor-suppressing effects of miR-411 overexpression on the proliferation and invasion of cervical cancer cells. In conclusion, our data demonstrated that miR-411 inhibited cervical cancer progression by directly targeting STAT3 and may represent a novel potential therapeutic target and prognostic marker for patients with this disease. Cognizant Communication Corporation 2019-02-21 /pmc/articles/PMC7848402/ /pubmed/29716674 http://dx.doi.org/10.3727/096504018X15247361080118 Text en Copyright © 2019 Cognizant, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License.
spellingShingle Article
Shan, Dan
Shang, Yumin
Hu, Tongxiu
MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title_full MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title_fullStr MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title_full_unstemmed MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title_short MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3
title_sort microrna-411 inhibits cervical cancer progression by directly targeting stat3
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848402/
https://www.ncbi.nlm.nih.gov/pubmed/29716674
http://dx.doi.org/10.3727/096504018X15247361080118
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