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MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1
BACKGROUND: Growing evidence suggests that microRNAs (miRNAs) play an important role in tumor development, progression and metastasis. Aberrant miR-106b expression has been reported in several cancers. However, the role and underlying mechanism of miR-106 in colorectal cancer (CRC) have not been add...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4520100/ https://www.ncbi.nlm.nih.gov/pubmed/26223867 http://dx.doi.org/10.1186/s13046-015-0189-7 |
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author | Zhang, Guang-jun Li, Jian-shui Zhou, He Xiao, Hua-xu Li, Yu Zhou, Tong |
author_facet | Zhang, Guang-jun Li, Jian-shui Zhou, He Xiao, Hua-xu Li, Yu Zhou, Tong |
author_sort | Zhang, Guang-jun |
collection | PubMed |
description | BACKGROUND: Growing evidence suggests that microRNAs (miRNAs) play an important role in tumor development, progression and metastasis. Aberrant miR-106b expression has been reported in several cancers. However, the role and underlying mechanism of miR-106 in colorectal cancer (CRC) have not been addressed. METHODS: Quantitative RT-PCR(qRT-PCR) was performed to evaluate miR-106b levels in CRC cell lines and patient specimens. Cell proliferation was detected using MTT assay, and cell migration and invasion ability were evaluated by wound healing assay and transwell assay. The target gene of miR-106b was determined by qRT-PCR, western blot and luciferase assays. RESULTS: miR-106b was significantly up-regulated in metastatic CRC tissues and cell lines, and high miR-106b expression was associated with lymph node metastasis and advanced clinical stage. In addition, miR-106b overexpression enhances, whereas miR-106b depletion reduces CRC cell migration and invasion. Moreover, we identify DLC1 as a direct target of miR-106b, reveal its expression to be inversely correlated with miR-106b in CRC samples and show that its re-introduction reverses miR-106b-induced CRC cell migration and invasion. Furthermore, survival analyses showed the patients with high mi-106b/low DLC1 had shorter overall survival (OS) and disease-free survival (DFS) rates, and confirmed miR-106b may be an independent prognostic factor for OS and DFS in CRC patients. CONCLUSIONS: Our findings indicate that miR-106b promotes CRC cell migration and invasion by targeting DLC1. This miRNA may serve as a potential prognostic biomarker and therapeutic target for CRC. |
format | Online Article Text |
id | pubmed-4520100 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-45201002015-07-31 MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 Zhang, Guang-jun Li, Jian-shui Zhou, He Xiao, Hua-xu Li, Yu Zhou, Tong J Exp Clin Cancer Res Research BACKGROUND: Growing evidence suggests that microRNAs (miRNAs) play an important role in tumor development, progression and metastasis. Aberrant miR-106b expression has been reported in several cancers. However, the role and underlying mechanism of miR-106 in colorectal cancer (CRC) have not been addressed. METHODS: Quantitative RT-PCR(qRT-PCR) was performed to evaluate miR-106b levels in CRC cell lines and patient specimens. Cell proliferation was detected using MTT assay, and cell migration and invasion ability were evaluated by wound healing assay and transwell assay. The target gene of miR-106b was determined by qRT-PCR, western blot and luciferase assays. RESULTS: miR-106b was significantly up-regulated in metastatic CRC tissues and cell lines, and high miR-106b expression was associated with lymph node metastasis and advanced clinical stage. In addition, miR-106b overexpression enhances, whereas miR-106b depletion reduces CRC cell migration and invasion. Moreover, we identify DLC1 as a direct target of miR-106b, reveal its expression to be inversely correlated with miR-106b in CRC samples and show that its re-introduction reverses miR-106b-induced CRC cell migration and invasion. Furthermore, survival analyses showed the patients with high mi-106b/low DLC1 had shorter overall survival (OS) and disease-free survival (DFS) rates, and confirmed miR-106b may be an independent prognostic factor for OS and DFS in CRC patients. CONCLUSIONS: Our findings indicate that miR-106b promotes CRC cell migration and invasion by targeting DLC1. This miRNA may serve as a potential prognostic biomarker and therapeutic target for CRC. BioMed Central 2015-07-30 /pmc/articles/PMC4520100/ /pubmed/26223867 http://dx.doi.org/10.1186/s13046-015-0189-7 Text en © Zhang et al. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zhang, Guang-jun Li, Jian-shui Zhou, He Xiao, Hua-xu Li, Yu Zhou, Tong MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title | MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title_full | MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title_fullStr | MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title_full_unstemmed | MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title_short | MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1 |
title_sort | microrna-106b promotes colorectal cancer cell migration and invasion by directly targeting dlc1 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4520100/ https://www.ncbi.nlm.nih.gov/pubmed/26223867 http://dx.doi.org/10.1186/s13046-015-0189-7 |
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