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Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors

Although dysregulation of microRNAs (miRNAs/miRs) is a common feature of human malignancies, its involvement in gastrointestinal stromal tumors (GISTs) is not fully understood. The present study aimed to identify the miRNAs that perform a role in GIST metastasis. miRNA expression profiles from a ser...

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Autores principales: Niinuma, Takeshi, Kai, Masahiro, Kitajima, Hiroshi, Yamamoto, Eiichiro, Harada, Taku, Maruyama, Reo, Nobuoka, Takayuki, Nishida, Toshirou, Kanda, Tatsuo, Hasegawa, Tadashi, Tokino, Takashi, Sugai, Tamotsu, Shinomura, Yasuhisa, Nakase, Hiroshi, Suzuki, Hiromu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661378/
https://www.ncbi.nlm.nih.gov/pubmed/29113198
http://dx.doi.org/10.3892/ol.2017.6911
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author Niinuma, Takeshi
Kai, Masahiro
Kitajima, Hiroshi
Yamamoto, Eiichiro
Harada, Taku
Maruyama, Reo
Nobuoka, Takayuki
Nishida, Toshirou
Kanda, Tatsuo
Hasegawa, Tadashi
Tokino, Takashi
Sugai, Tamotsu
Shinomura, Yasuhisa
Nakase, Hiroshi
Suzuki, Hiromu
author_facet Niinuma, Takeshi
Kai, Masahiro
Kitajima, Hiroshi
Yamamoto, Eiichiro
Harada, Taku
Maruyama, Reo
Nobuoka, Takayuki
Nishida, Toshirou
Kanda, Tatsuo
Hasegawa, Tadashi
Tokino, Takashi
Sugai, Tamotsu
Shinomura, Yasuhisa
Nakase, Hiroshi
Suzuki, Hiromu
author_sort Niinuma, Takeshi
collection PubMed
description Although dysregulation of microRNAs (miRNAs/miRs) is a common feature of human malignancies, its involvement in gastrointestinal stromal tumors (GISTs) is not fully understood. The present study aimed to identify the miRNAs that perform a role in GIST metastasis. miRNA expression profiles from a series of 32 primary GISTs were analyzed using microarrays, and miR-186 was observed to be downregulated in tumors exhibiting metastatic recurrence. Reverse transcription-quantitative polymerase chain reaction analysis of an independent cohort of 100 primary GISTs revealed that low miR-186 expression is associated with metastatic recurrence and a poor prognosis. Inhibition of miR-186 in GIST-T1 cells promoted cell migration. Gene expression microarray analysis demonstrated that miR-186 inhibition upregulated a set of genes implicated in cancer metastasis, including insulin-like growth factor-binding protein 3, AKT serine/threonine kinase 2, hepatocyte growth factor receptor, CXC chemokine receptor 4 and epidermal growth factor-containing fibulin-like extracellular matrix protein 1. These results suggest that the downregulation of miR-186 is involved in the metastatic recurrence of GISTs, and that miR-186 levels could potentially be a predictive biomarker for clinical outcome.
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spelling pubmed-56613782017-11-06 Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors Niinuma, Takeshi Kai, Masahiro Kitajima, Hiroshi Yamamoto, Eiichiro Harada, Taku Maruyama, Reo Nobuoka, Takayuki Nishida, Toshirou Kanda, Tatsuo Hasegawa, Tadashi Tokino, Takashi Sugai, Tamotsu Shinomura, Yasuhisa Nakase, Hiroshi Suzuki, Hiromu Oncol Lett Articles Although dysregulation of microRNAs (miRNAs/miRs) is a common feature of human malignancies, its involvement in gastrointestinal stromal tumors (GISTs) is not fully understood. The present study aimed to identify the miRNAs that perform a role in GIST metastasis. miRNA expression profiles from a series of 32 primary GISTs were analyzed using microarrays, and miR-186 was observed to be downregulated in tumors exhibiting metastatic recurrence. Reverse transcription-quantitative polymerase chain reaction analysis of an independent cohort of 100 primary GISTs revealed that low miR-186 expression is associated with metastatic recurrence and a poor prognosis. Inhibition of miR-186 in GIST-T1 cells promoted cell migration. Gene expression microarray analysis demonstrated that miR-186 inhibition upregulated a set of genes implicated in cancer metastasis, including insulin-like growth factor-binding protein 3, AKT serine/threonine kinase 2, hepatocyte growth factor receptor, CXC chemokine receptor 4 and epidermal growth factor-containing fibulin-like extracellular matrix protein 1. These results suggest that the downregulation of miR-186 is involved in the metastatic recurrence of GISTs, and that miR-186 levels could potentially be a predictive biomarker for clinical outcome. D.A. Spandidos 2017-11 2017-09-08 /pmc/articles/PMC5661378/ /pubmed/29113198 http://dx.doi.org/10.3892/ol.2017.6911 Text en Copyright: © Niinuma 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
Niinuma, Takeshi
Kai, Masahiro
Kitajima, Hiroshi
Yamamoto, Eiichiro
Harada, Taku
Maruyama, Reo
Nobuoka, Takayuki
Nishida, Toshirou
Kanda, Tatsuo
Hasegawa, Tadashi
Tokino, Takashi
Sugai, Tamotsu
Shinomura, Yasuhisa
Nakase, Hiroshi
Suzuki, Hiromu
Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title_full Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title_fullStr Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title_full_unstemmed Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title_short Downregulation of miR-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
title_sort downregulation of mir-186 is associated with metastatic recurrence of gastrointestinal stromal tumors
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661378/
https://www.ncbi.nlm.nih.gov/pubmed/29113198
http://dx.doi.org/10.3892/ol.2017.6911
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