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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...

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Autores principales: He, Qingmei, Ren, Xianyue, Chen, Jiewei, Li, Yingqin, Tang, Xinran, Wen, Xin, Yang, Xiaojing, Zhang, Jian, Wang, Yaqin, Ma, Jun, Liu, Na
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
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.
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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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