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miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways
Dysregulation of miRNAs has been shown to contribute to the carcinogenesis and progression of nasopharyngeal carcinoma (NPC). Our previous microarray data showed that miR-16 expression is significantly decreased in archived NPC tissues. Here, we confirmed that miR-16 was reduced in NPC cell lines an...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823089/ https://www.ncbi.nlm.nih.gov/pubmed/26655091 http://dx.doi.org/10.18632/oncotarget.6504 |
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author | He, Qingmei Ren, Xianyue Chen, Jiewei Li, Yingqin Tang, Xinran Wen, Xin Yang, Xiaojing Zhang, Jian Wang, Yaqin Ma, Jun Liu, Na |
author_facet | He, Qingmei Ren, Xianyue Chen, Jiewei Li, Yingqin Tang, Xinran Wen, Xin Yang, Xiaojing Zhang, Jian Wang, Yaqin Ma, Jun Liu, Na |
author_sort | He, Qingmei |
collection | PubMed |
description | Dysregulation of miRNAs has been shown to contribute to the carcinogenesis and progression of nasopharyngeal carcinoma (NPC). Our previous microarray data showed that miR-16 expression is significantly decreased in archived NPC tissues. Here, we confirmed that miR-16 was reduced in NPC cell lines and freshly-frozen samples. Ectopic expression of miR-16 suppressed NPC cell proliferation, migration, and invasion in vitro and inhibited tumor growth and metastatic colonization in the lung in vivo. Furthermore, fibroblast growth factor 2 (FGF2) was identified as a direct target of miR-16, and both phosphoinositide-3- kinase/AKT (PI3K/AKT) and mitogen-activated protein kinase (MAPK) signaling pathways were repressed after miR-16 overexpression. In addition, the restoration of FGF2 reversed the suppressive effects of miR-16. Together, these results indicated that miR-16 suppresses NPC carcinogenesis and progression by targeting FGF2, thereby representing a potential target for miRNA-based therapy for NPC in the future. |
format | Online Article Text |
id | pubmed-4823089 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-48230892016-05-03 miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways He, Qingmei Ren, Xianyue Chen, Jiewei Li, Yingqin Tang, Xinran Wen, Xin Yang, Xiaojing Zhang, Jian Wang, Yaqin Ma, Jun Liu, Na Oncotarget Research Paper Dysregulation of miRNAs has been shown to contribute to the carcinogenesis and progression of nasopharyngeal carcinoma (NPC). Our previous microarray data showed that miR-16 expression is significantly decreased in archived NPC tissues. Here, we confirmed that miR-16 was reduced in NPC cell lines and freshly-frozen samples. Ectopic expression of miR-16 suppressed NPC cell proliferation, migration, and invasion in vitro and inhibited tumor growth and metastatic colonization in the lung in vivo. Furthermore, fibroblast growth factor 2 (FGF2) was identified as a direct target of miR-16, and both phosphoinositide-3- kinase/AKT (PI3K/AKT) and mitogen-activated protein kinase (MAPK) signaling pathways were repressed after miR-16 overexpression. In addition, the restoration of FGF2 reversed the suppressive effects of miR-16. Together, these results indicated that miR-16 suppresses NPC carcinogenesis and progression by targeting FGF2, thereby representing a potential target for miRNA-based therapy for NPC in the future. Impact Journals LLC 2015-12-08 /pmc/articles/PMC4823089/ /pubmed/26655091 http://dx.doi.org/10.18632/oncotarget.6504 Text en Copyright: © 2016 He et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper He, Qingmei Ren, Xianyue Chen, Jiewei Li, Yingqin Tang, Xinran Wen, Xin Yang, Xiaojing Zhang, Jian Wang, Yaqin Ma, Jun Liu, Na miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title | miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title_full | miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title_fullStr | miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title_full_unstemmed | miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title_short | miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways |
title_sort | mir-16 targets fibroblast growth factor 2 to inhibit npc cell proliferation and invasion via pi3k/akt and mapk signaling pathways |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823089/ https://www.ncbi.nlm.nih.gov/pubmed/26655091 http://dx.doi.org/10.18632/oncotarget.6504 |
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