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miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC

Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-12...

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Autores principales: Xia, Yang, Wei, Ke, Yang, Feng-Ming, Hu, Liu-Qing, Pan, Chun-Feng, Pan, Xiang-Long, Wu, Wei-Bing, Wang, Jun, Wen, Wei, He, Zhi-Cheng, Xu, Jing, Xu, Xin-Feng, Zhu, Quan, Chen, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368632/
https://www.ncbi.nlm.nih.gov/pubmed/30737371
http://dx.doi.org/10.1038/s41419-019-1390-y
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author Xia, Yang
Wei, Ke
Yang, Feng-Ming
Hu, Liu-Qing
Pan, Chun-Feng
Pan, Xiang-Long
Wu, Wei-Bing
Wang, Jun
Wen, Wei
He, Zhi-Cheng
Xu, Jing
Xu, Xin-Feng
Zhu, Quan
Chen, Liang
author_facet Xia, Yang
Wei, Ke
Yang, Feng-Ming
Hu, Liu-Qing
Pan, Chun-Feng
Pan, Xiang-Long
Wu, Wei-Bing
Wang, Jun
Wen, Wei
He, Zhi-Cheng
Xu, Jing
Xu, Xin-Feng
Zhu, Quan
Chen, Liang
author_sort Xia, Yang
collection PubMed
description Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3′-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis.
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spelling pubmed-63686322019-02-11 miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC Xia, Yang Wei, Ke Yang, Feng-Ming Hu, Liu-Qing Pan, Chun-Feng Pan, Xiang-Long Wu, Wei-Bing Wang, Jun Wen, Wei He, Zhi-Cheng Xu, Jing Xu, Xin-Feng Zhu, Quan Chen, Liang Cell Death Dis Article Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3′-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis. Nature Publishing Group UK 2019-02-08 /pmc/articles/PMC6368632/ /pubmed/30737371 http://dx.doi.org/10.1038/s41419-019-1390-y Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Xia, Yang
Wei, Ke
Yang, Feng-Ming
Hu, Liu-Qing
Pan, Chun-Feng
Pan, Xiang-Long
Wu, Wei-Bing
Wang, Jun
Wen, Wei
He, Zhi-Cheng
Xu, Jing
Xu, Xin-Feng
Zhu, Quan
Chen, Liang
miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title_full miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title_fullStr miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title_full_unstemmed miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title_short miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
title_sort mir-1260b, mediated by yy1, activates kit signaling by targeting socs6 to regulate cell proliferation and apoptosis in nsclc
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368632/
https://www.ncbi.nlm.nih.gov/pubmed/30737371
http://dx.doi.org/10.1038/s41419-019-1390-y
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