miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2
Colorectal cancer (CRC) is one of the most common cancers worldwide, with a particularly high incidence in developed countries. Distant metastasis and recurrence are the main causes of CRC-related deaths. MicroRNAs (miRNAs) in the serum make them potential biomarkers for cancers, as reported in seru...
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pubmed-46507312015-12-02 miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 Sheng, L He, P Yang, X Zhou, M Feng, Q Original Article Colorectal cancer (CRC) is one of the most common cancers worldwide, with a particularly high incidence in developed countries. Distant metastasis and recurrence are the main causes of CRC-related deaths. MicroRNAs (miRNAs) in the serum make them potential biomarkers for cancers, as reported in serum or tumor tissues from CRC patients. In this study, we found that miR-612 expression was significantly lower in CRC tissues or cells compared with peritumor tissues or normal cells, and lower in metastatic CRC specimens compared with non-metastatic specimens, whereas AKT2 exhibited opposite trend. Gain-of-function and loss-of-function assays showed that miR-612 inhibited CRC cell proliferation and migration in vitro by Cell Counting Kit-8 and transwell assays. Further analysis revealed that miR-612 directly suppressed AKT2, which in turn inhibited the downstream epithelial–mesenchymal transition-related signaling pathway. These results were additionally validated in vivo by tumorigenesis and liver metastasis experiments. The results of this study suggested a critical role of miR-612 in the development of CRC. Nature Publishing Group 2015-07 2015-07-09 /pmc/articles/PMC4650731/ /pubmed/26158514 http://dx.doi.org/10.1038/cddis.2015.184 Text en Copyright © 2015 Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Sheng, L He, P Yang, X Zhou, M Feng, Q |
spellingShingle |
Sheng, L He, P Yang, X Zhou, M Feng, Q miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
author_facet |
Sheng, L He, P Yang, X Zhou, M Feng, Q |
author_sort |
Sheng, L |
title |
miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
title_short |
miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
title_full |
miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
title_fullStr |
miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
title_full_unstemmed |
miR-612 negatively regulates colorectal cancer growth and metastasis by targeting AKT2 |
title_sort |
mir-612 negatively regulates colorectal cancer growth and metastasis by targeting akt2 |
description |
Colorectal cancer (CRC) is one of the most common cancers worldwide, with a particularly high incidence in developed countries. Distant metastasis and recurrence are the main causes of CRC-related deaths. MicroRNAs (miRNAs) in the serum make them potential biomarkers for cancers, as reported in serum or tumor tissues from CRC patients. In this study, we found that miR-612 expression was significantly lower in CRC tissues or cells compared with peritumor tissues or normal cells, and lower in metastatic CRC specimens compared with non-metastatic specimens, whereas AKT2 exhibited opposite trend. Gain-of-function and loss-of-function assays showed that miR-612 inhibited CRC cell proliferation and migration in vitro by Cell Counting Kit-8 and transwell assays. Further analysis revealed that miR-612 directly suppressed AKT2, which in turn inhibited the downstream epithelial–mesenchymal transition-related signaling pathway. These results were additionally validated in vivo by tumorigenesis and liver metastasis experiments. The results of this study suggested a critical role of miR-612 in the development of CRC. |
publisher |
Nature Publishing Group |
publishDate |
2015 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650731/ |
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1613503209312092160 |