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MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP
In the present study, the function of miR-150 and its downstream target iASPP in the growth and metastasis of colorectal cancer (CRC) cells was investigated. The expression of miR-150 and iASPP was first investigated in clinical CRC samples. Subsequently, the effects of miR-150 overexpression and iA...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059748/ https://www.ncbi.nlm.nih.gov/pubmed/29750311 http://dx.doi.org/10.3892/or.2018.6406 |
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author | Li, Chen Du, Xiaohui Xia, Shaoyou Chen, Lin |
author_facet | Li, Chen Du, Xiaohui Xia, Shaoyou Chen, Lin |
author_sort | Li, Chen |
collection | PubMed |
description | In the present study, the function of miR-150 and its downstream target iASPP in the growth and metastasis of colorectal cancer (CRC) cells was investigated. The expression of miR-150 and iASPP was first investigated in clinical CRC samples. Subsequently, the effects of miR-150 overexpression and iASPP inhibition on cell viability, cell cycle distribution, apoptosis, migration and invasion were detected with CCK-8, flow cytometry, scratch and Transwell assays. The interaction between miR-150 and iASPP was confirmed using a dual-luciferase assay. Subsequently, the key role of iASPP in the anti-CRC function of miR-150 was assessed by inducing the expression of the gene in miR-150 overexpressed SW480 cells. In clinical samples, the level of miR-150 was downregulated, while iASPP was induced. Enforced expression of miR-150 decreased the viability, induced G1 cell cycle arrest and apoptosis, and inhibited the migration and invasion of SW480 cells. Knockdown of iASPP exerted a similar effect on SW480 cells to that of the overexpression of miR-150. Dual-luciferase assay demonstrated that miR-150 directly bound to iASPP and inhibited its transcription. The function of miR-150 depended on the inhibition of iASPP; induced expression of iASPP in miR-150-knockdown SW480 and HCT116 cells restored cell viability, migration and invasion while inhibiting G1 cell cycle arrest and apoptosis. Increased expression of miR-150 suppressed viability, proliferation, migration and invasion of SW480 cells. Furthermore, iASPP was a direct target of miR-150 and played a key role in its anti-CRC function. miR-150 may be a promising predictor of prognosis in CRC patients. |
format | Online Article Text |
id | pubmed-6059748 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60597482018-07-26 MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP Li, Chen Du, Xiaohui Xia, Shaoyou Chen, Lin Oncol Rep Articles In the present study, the function of miR-150 and its downstream target iASPP in the growth and metastasis of colorectal cancer (CRC) cells was investigated. The expression of miR-150 and iASPP was first investigated in clinical CRC samples. Subsequently, the effects of miR-150 overexpression and iASPP inhibition on cell viability, cell cycle distribution, apoptosis, migration and invasion were detected with CCK-8, flow cytometry, scratch and Transwell assays. The interaction between miR-150 and iASPP was confirmed using a dual-luciferase assay. Subsequently, the key role of iASPP in the anti-CRC function of miR-150 was assessed by inducing the expression of the gene in miR-150 overexpressed SW480 cells. In clinical samples, the level of miR-150 was downregulated, while iASPP was induced. Enforced expression of miR-150 decreased the viability, induced G1 cell cycle arrest and apoptosis, and inhibited the migration and invasion of SW480 cells. Knockdown of iASPP exerted a similar effect on SW480 cells to that of the overexpression of miR-150. Dual-luciferase assay demonstrated that miR-150 directly bound to iASPP and inhibited its transcription. The function of miR-150 depended on the inhibition of iASPP; induced expression of iASPP in miR-150-knockdown SW480 and HCT116 cells restored cell viability, migration and invasion while inhibiting G1 cell cycle arrest and apoptosis. Increased expression of miR-150 suppressed viability, proliferation, migration and invasion of SW480 cells. Furthermore, iASPP was a direct target of miR-150 and played a key role in its anti-CRC function. miR-150 may be a promising predictor of prognosis in CRC patients. D.A. Spandidos 2018-07 2018-04-30 /pmc/articles/PMC6059748/ /pubmed/29750311 http://dx.doi.org/10.3892/or.2018.6406 Text en Copyright: © Li 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 Li, Chen Du, Xiaohui Xia, Shaoyou Chen, Lin MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title | MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title_full | MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title_fullStr | MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title_full_unstemmed | MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title_short | MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP |
title_sort | microrna-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iaspp |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059748/ https://www.ncbi.nlm.nih.gov/pubmed/29750311 http://dx.doi.org/10.3892/or.2018.6406 |
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