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Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis
Colorectal cancer (CRC) is one of the most aggressive malignancies worldwide. Increasing evidence has indicated that microRNA (miR)-599 is involved in the occurrence and development of different types of tumors, such as breast cancer and glioma. However, the role of miR-599 in CRC remains unclear. T...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7856695/ https://www.ncbi.nlm.nih.gov/pubmed/33613714 http://dx.doi.org/10.3892/ol.2021.12486 |
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author | Yu, You Lai, Suhe Peng, Xiaochao |
author_facet | Yu, You Lai, Suhe Peng, Xiaochao |
author_sort | Yu, You |
collection | PubMed |
description | Colorectal cancer (CRC) is one of the most aggressive malignancies worldwide. Increasing evidence has indicated that microRNA (miR)-599 is involved in the occurrence and development of different types of tumors, such as breast cancer and glioma. However, the role of miR-599 in CRC remains unclear. Thus, the present study aimed to identify the regulatory mechanism of miR-599 in CRC progression. Reverse transcription-quantitative PCR was used to analyze the expression levels of MCM3AP-AS1, miR-599 and ARPP19, and Cell Counting Kit-8 and Transwell assays were used to determine the cell proliferation and migration of CRC cells. In addition, a Dual-luciferase reporter assay was used to analyze the direct interaction between miR-599 and MCM3AP-AS1 or ARPP19. Reverse transcription-quantitative PCR analysis demonstrated that miR-599 expression decreased in patients with CRC and in CRC cell lines, while miR-599 overexpression inhibited cell proliferation and migration abilities in vitro. MCM3AP-AS1 was identified as a molecular sponge of miR-599, and further investigation indicated that MCM3AP-AS1 silencing inhibited cell proliferation and migration of the CRC cell lines. In addition, ARPP19 was identified as a target gene of miR-599, and MCM3AP-AS1-knockdown decreased ARPP19 mRNA expression and increased miR-599 expression. Furthermore, silencing ARPP19 inhibited the proliferation and migration of the CRC cell lines. The results also demonstrated that MCM3AP-AS1 promoted CRC cell progression by regulating the miR-599/ARPP19 axis. Taken together, the results of the present study suggest that MCM3AP-AS1 may be a novel therapeutic target for patients with CRC. |
format | Online Article Text |
id | pubmed-7856695 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-78566952021-02-18 Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis Yu, You Lai, Suhe Peng, Xiaochao Oncol Lett Articles Colorectal cancer (CRC) is one of the most aggressive malignancies worldwide. Increasing evidence has indicated that microRNA (miR)-599 is involved in the occurrence and development of different types of tumors, such as breast cancer and glioma. However, the role of miR-599 in CRC remains unclear. Thus, the present study aimed to identify the regulatory mechanism of miR-599 in CRC progression. Reverse transcription-quantitative PCR was used to analyze the expression levels of MCM3AP-AS1, miR-599 and ARPP19, and Cell Counting Kit-8 and Transwell assays were used to determine the cell proliferation and migration of CRC cells. In addition, a Dual-luciferase reporter assay was used to analyze the direct interaction between miR-599 and MCM3AP-AS1 or ARPP19. Reverse transcription-quantitative PCR analysis demonstrated that miR-599 expression decreased in patients with CRC and in CRC cell lines, while miR-599 overexpression inhibited cell proliferation and migration abilities in vitro. MCM3AP-AS1 was identified as a molecular sponge of miR-599, and further investigation indicated that MCM3AP-AS1 silencing inhibited cell proliferation and migration of the CRC cell lines. In addition, ARPP19 was identified as a target gene of miR-599, and MCM3AP-AS1-knockdown decreased ARPP19 mRNA expression and increased miR-599 expression. Furthermore, silencing ARPP19 inhibited the proliferation and migration of the CRC cell lines. The results also demonstrated that MCM3AP-AS1 promoted CRC cell progression by regulating the miR-599/ARPP19 axis. Taken together, the results of the present study suggest that MCM3AP-AS1 may be a novel therapeutic target for patients with CRC. D.A. Spandidos 2021-03 2021-01-24 /pmc/articles/PMC7856695/ /pubmed/33613714 http://dx.doi.org/10.3892/ol.2021.12486 Text en Copyright: © Yu 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 Yu, You Lai, Suhe Peng, Xiaochao Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title | Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title_full | Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title_fullStr | Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title_full_unstemmed | Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title_short | Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis |
title_sort | long non-coding rna mcm3ap-as1 facilitates colorectal cancer progression by regulating the microrna-599/arpp19 axis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7856695/ https://www.ncbi.nlm.nih.gov/pubmed/33613714 http://dx.doi.org/10.3892/ol.2021.12486 |
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