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STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway
PURPOSE: Colorectal carcinoma (CRC) is among the most common causes of death. Recent studies have shown that both STAT3 and miR-572 contribute to CRC progression. STAT3 plays an important role in miRNA expression. Moreover, MOAP-1, which is a pro-apoptotic protein that induces cell death or apoptosi...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007208/ https://www.ncbi.nlm.nih.gov/pubmed/29942139 http://dx.doi.org/10.2147/OTT.S158764 |
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author | Wang, Nan He, Xianli Zhou, Ru Jia, Guozhan Qiao, Qing |
author_facet | Wang, Nan He, Xianli Zhou, Ru Jia, Guozhan Qiao, Qing |
author_sort | Wang, Nan |
collection | PubMed |
description | PURPOSE: Colorectal carcinoma (CRC) is among the most common causes of death. Recent studies have shown that both STAT3 and miR-572 contribute to CRC progression. STAT3 plays an important role in miRNA expression. Moreover, MOAP-1, which is a pro-apoptotic protein that induces cell death or apoptosis, has a direct correlation with miRNA. Therefore, the current study is designed to explore whether miR-572 and STAT3 are involved in a common pathway and the role of MOAP-1 in this process. PATIENTS AND METHODS: The expressions of STAT3, miR-572, and MOAP-1 in human CRC tissues and multiple cell lines were estimated by qRT-PCR or Western blot. MTT, transwell migration, and invasion assays were used to assess cell growth, migration, and invasion, respectively. Dual-luciferase reporter assay was applied to examine the association between miR-572 and MOAP-1. RESULTS: Elevated STAT3 levels were accompanied by increased miR-572 and decreased MOAP-1 levels in primary CRC specimens and cell lines. STAT3 promoted CRC cell growth, migration, and invasion via the upregulated expression of miR-572. Subsequently, miR-572 inhibited MOAP-1 protein expression through an interaction with its 3′UTR. CONCLUSION: Our study proposes a novel STAT3-miR-572-MOAP-1 pathway involved in the process of CRC progression, which might be a potential target for the development of new preventive and therapeutic approaches against human colorectal cancer. |
format | Online Article Text |
id | pubmed-6007208 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-60072082018-06-25 STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway Wang, Nan He, Xianli Zhou, Ru Jia, Guozhan Qiao, Qing Onco Targets Ther Original Research PURPOSE: Colorectal carcinoma (CRC) is among the most common causes of death. Recent studies have shown that both STAT3 and miR-572 contribute to CRC progression. STAT3 plays an important role in miRNA expression. Moreover, MOAP-1, which is a pro-apoptotic protein that induces cell death or apoptosis, has a direct correlation with miRNA. Therefore, the current study is designed to explore whether miR-572 and STAT3 are involved in a common pathway and the role of MOAP-1 in this process. PATIENTS AND METHODS: The expressions of STAT3, miR-572, and MOAP-1 in human CRC tissues and multiple cell lines were estimated by qRT-PCR or Western blot. MTT, transwell migration, and invasion assays were used to assess cell growth, migration, and invasion, respectively. Dual-luciferase reporter assay was applied to examine the association between miR-572 and MOAP-1. RESULTS: Elevated STAT3 levels were accompanied by increased miR-572 and decreased MOAP-1 levels in primary CRC specimens and cell lines. STAT3 promoted CRC cell growth, migration, and invasion via the upregulated expression of miR-572. Subsequently, miR-572 inhibited MOAP-1 protein expression through an interaction with its 3′UTR. CONCLUSION: Our study proposes a novel STAT3-miR-572-MOAP-1 pathway involved in the process of CRC progression, which might be a potential target for the development of new preventive and therapeutic approaches against human colorectal cancer. Dove Medical Press 2018-06-15 /pmc/articles/PMC6007208/ /pubmed/29942139 http://dx.doi.org/10.2147/OTT.S158764 Text en © 2018 Wang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Wang, Nan He, Xianli Zhou, Ru Jia, Guozhan Qiao, Qing STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title | STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title_full | STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title_fullStr | STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title_full_unstemmed | STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title_short | STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway |
title_sort | stat3 induces colorectal carcinoma progression through a novel mir-572-moap-1 pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007208/ https://www.ncbi.nlm.nih.gov/pubmed/29942139 http://dx.doi.org/10.2147/OTT.S158764 |
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