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MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells
MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular me...
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/PMC4695027/ https://www.ncbi.nlm.nih.gov/pubmed/26314959 |
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author | Zheng, Hailun Ma, Renqiang Wang, Qizhi Zhang, Pei Li, Dapeng Wang, Qiangwu Wang, Jianchao Li, Huabin Liu, Hao Wang, Zhiwei |
author_facet | Zheng, Hailun Ma, Renqiang Wang, Qizhi Zhang, Pei Li, Dapeng Wang, Qiangwu Wang, Jianchao Li, Huabin Liu, Hao Wang, Zhiwei |
author_sort | Zheng, Hailun |
collection | PubMed |
description | MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular mechanisms of miR-625-3p-mediated tumorigenesis are largely elusive. Therefore, the aim of this study was to evaluate the biological function and molecular insight on miR-625-3p-induced oncogenesis in colorectal carcinoma (CRC). The effects of miR-625-3p in cell migration and invasion were analyzed by wound healing assay and transwell assay, respectively. In addition, the expression of miR-625-3p and its targets was detected in five human CRC cell lines. In the present study, we found that overexpression of miR-625-3p promoted migration and invasion in SW480 cells, whereas downregulation of miR-625-3p inhibited cell motility in SW620 cells. More importantly, we observed potential binding sites for miR-625-3p in the 3′-untranslated region of suppressor of cancer cell invasion (SCAI). Notably, we identified that overexpression of miR-625-3p inhibited the expression of SCAI, while depletion of miR-625-3p increased SCAI level, suggesting that SCAI could be a target of miR-625-3p. Additionally, we revealed that miR-625-3p exerts its oncogenic functions through regulation of SCAI/E-cadherin/MMP-9 pathways. Our findings indicate the pivotal role of miR-625-3p in invasion that warrants further exploration whether targeting miR-625-3p could be a promising approach for the treatment of CRC. |
format | Online Article Text |
id | pubmed-4695027 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-46950272016-01-20 MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells Zheng, Hailun Ma, Renqiang Wang, Qizhi Zhang, Pei Li, Dapeng Wang, Qiangwu Wang, Jianchao Li, Huabin Liu, Hao Wang, Zhiwei Oncotarget Research Paper MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular mechanisms of miR-625-3p-mediated tumorigenesis are largely elusive. Therefore, the aim of this study was to evaluate the biological function and molecular insight on miR-625-3p-induced oncogenesis in colorectal carcinoma (CRC). The effects of miR-625-3p in cell migration and invasion were analyzed by wound healing assay and transwell assay, respectively. In addition, the expression of miR-625-3p and its targets was detected in five human CRC cell lines. In the present study, we found that overexpression of miR-625-3p promoted migration and invasion in SW480 cells, whereas downregulation of miR-625-3p inhibited cell motility in SW620 cells. More importantly, we observed potential binding sites for miR-625-3p in the 3′-untranslated region of suppressor of cancer cell invasion (SCAI). Notably, we identified that overexpression of miR-625-3p inhibited the expression of SCAI, while depletion of miR-625-3p increased SCAI level, suggesting that SCAI could be a target of miR-625-3p. Additionally, we revealed that miR-625-3p exerts its oncogenic functions through regulation of SCAI/E-cadherin/MMP-9 pathways. Our findings indicate the pivotal role of miR-625-3p in invasion that warrants further exploration whether targeting miR-625-3p could be a promising approach for the treatment of CRC. Impact Journals LLC 2015-07-28 /pmc/articles/PMC4695027/ /pubmed/26314959 Text en Copyright: © 2015 Zheng 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 Zheng, Hailun Ma, Renqiang Wang, Qizhi Zhang, Pei Li, Dapeng Wang, Qiangwu Wang, Jianchao Li, Huabin Liu, Hao Wang, Zhiwei MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title | MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title_full | MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title_fullStr | MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title_full_unstemmed | MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title_short | MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells |
title_sort | mir-625-3p promotes cell migration and invasion via inhibition of scai in colorectal carcinoma cells |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695027/ https://www.ncbi.nlm.nih.gov/pubmed/26314959 |
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