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miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9

Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progress...

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Autores principales: Ma, Jun, Tong, Hong-Feng, Lin, Jie-Huan, Chen, Fu-Nan, Wu, Can-Xing, Cao, Cheng-Zhang, Wu, Jian, Hu, Shu-Qiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285925/
https://www.ncbi.nlm.nih.gov/pubmed/32565956
http://dx.doi.org/10.3892/ol.2020.11570
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author Ma, Jun
Tong, Hong-Feng
Lin, Jie-Huan
Chen, Fu-Nan
Wu, Can-Xing
Cao, Cheng-Zhang
Wu, Jian
Hu, Shu-Qiao
author_facet Ma, Jun
Tong, Hong-Feng
Lin, Jie-Huan
Chen, Fu-Nan
Wu, Can-Xing
Cao, Cheng-Zhang
Wu, Jian
Hu, Shu-Qiao
author_sort Ma, Jun
collection PubMed
description Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progression. A total of 62 pairs of primary tumor and adjacent normal tissues were collected from patients with NSCLC. miR-208b-5p expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-208b-5p mimics was transfected into NSCLC A549 and H1299 cells in order to upregulate miR-208b-5p expression. Dual-luciferase reporter assay was utilized to investigate the associations between miR-208b-5p and IL9 mRNA. The results demonstrated that miR-208b-5p expression decreased in NSCLC tissues and cell lines. Furthermore, miR-208b-5p overexpression inhibited A549 and H1299 cell proliferation and invasiveness. miR-208b-5p was demonstrated to bind directly to the 3′ untranslated region of interleukin-9 (IL-9) and therefore decreased its expression. In the NSCLC-derived cell lines, miR-208b-5p inactivated IL-9/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Furthermore, enhanced IL-9 level decreased the miR-208b-5p-mediated suppression of epithelial-mesenchymal transition in NSCLC cells by inactivating the STAT3 signaling pathway. In conclusion, the findings from this study demonstrated that miR-208b-5p inhibited migration and invasion of NSCLC cells. The anti-tumor activity of miR-208b-5p may be mediated by IL-9 and STAT-3 pathway.
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spelling pubmed-72859252020-06-18 miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9 Ma, Jun Tong, Hong-Feng Lin, Jie-Huan Chen, Fu-Nan Wu, Can-Xing Cao, Cheng-Zhang Wu, Jian Hu, Shu-Qiao Oncol Lett Articles Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progression. A total of 62 pairs of primary tumor and adjacent normal tissues were collected from patients with NSCLC. miR-208b-5p expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-208b-5p mimics was transfected into NSCLC A549 and H1299 cells in order to upregulate miR-208b-5p expression. Dual-luciferase reporter assay was utilized to investigate the associations between miR-208b-5p and IL9 mRNA. The results demonstrated that miR-208b-5p expression decreased in NSCLC tissues and cell lines. Furthermore, miR-208b-5p overexpression inhibited A549 and H1299 cell proliferation and invasiveness. miR-208b-5p was demonstrated to bind directly to the 3′ untranslated region of interleukin-9 (IL-9) and therefore decreased its expression. In the NSCLC-derived cell lines, miR-208b-5p inactivated IL-9/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Furthermore, enhanced IL-9 level decreased the miR-208b-5p-mediated suppression of epithelial-mesenchymal transition in NSCLC cells by inactivating the STAT3 signaling pathway. In conclusion, the findings from this study demonstrated that miR-208b-5p inhibited migration and invasion of NSCLC cells. The anti-tumor activity of miR-208b-5p may be mediated by IL-9 and STAT-3 pathway. D.A. Spandidos 2020-07 2020-04-23 /pmc/articles/PMC7285925/ /pubmed/32565956 http://dx.doi.org/10.3892/ol.2020.11570 Text en Copyright: © Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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 Articles
Ma, Jun
Tong, Hong-Feng
Lin, Jie-Huan
Chen, Fu-Nan
Wu, Can-Xing
Cao, Cheng-Zhang
Wu, Jian
Hu, Shu-Qiao
miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title_full miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title_fullStr miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title_full_unstemmed miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title_short miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9
title_sort mir-208b-5p inhibits invasion of non-small cell lung cancer through the stat3 pathway by targeting interleukin-9
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285925/
https://www.ncbi.nlm.nih.gov/pubmed/32565956
http://dx.doi.org/10.3892/ol.2020.11570
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