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NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway
Nuclear receptor subfamily 3, group C, member 2 (NR3C2) serves an antitumorigenic role in several types of cancer; however, its role and mechanisms of action in colon cancer remains to be elucidated. The aim of the present study was to explore the effects of NR3C2 on the proliferation, migration, in...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908346/ https://www.ncbi.nlm.nih.gov/pubmed/35191517 http://dx.doi.org/10.3892/mmr.2022.12649 |
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author | Li, Jia Xu, Zhao |
author_facet | Li, Jia Xu, Zhao |
author_sort | Li, Jia |
collection | PubMed |
description | Nuclear receptor subfamily 3, group C, member 2 (NR3C2) serves an antitumorigenic role in several types of cancer; however, its role and mechanisms of action in colon cancer remains to be elucidated. The aim of the present study was to explore the effects of NR3C2 on the proliferation, migration, invasion and angiogenesis of colon cancer cells. The expression levels of NR3C2 in human colon epithelial NCM460 cells (spontaneously immortalized cell line) and colon cancer cell lines was detected using reverse transcription-quantitative PCR and western blotting. Cell Counting Kit-8 (CCK-8) and colony formation assays were used to assess cell viability and wound healing and Transwell assays were used to detect cell invasion and migration. ELISA was used to detect the expression levels of VEGF and tube formation assays were used to assess angiogenesis. The expression levels of angiogenesis-related proteins and AKT/ERK signaling pathway-related proteins were detected by western blotting. NR3C2 expression was downregulated in colon cancer cells and overexpression of NR3C2 inhibited proliferation, colony formation, migration and invasion of colon cancer cells. Overexpression of NR3C2 inhibited angiogenesis and activity of the AKT/ERK signaling pathway in colon cancer cells. Thus, it was demonstrated that NR3C2 inhibited the proliferation, colony formation, migration, invasion and angiogenesis of colon cancer cells through the AKT/ERK signaling pathway. These results may highlight novel targets for the treatment of colon cancer. |
format | Online Article Text |
id | pubmed-8908346 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-89083462022-03-21 NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway Li, Jia Xu, Zhao Mol Med Rep Articles Nuclear receptor subfamily 3, group C, member 2 (NR3C2) serves an antitumorigenic role in several types of cancer; however, its role and mechanisms of action in colon cancer remains to be elucidated. The aim of the present study was to explore the effects of NR3C2 on the proliferation, migration, invasion and angiogenesis of colon cancer cells. The expression levels of NR3C2 in human colon epithelial NCM460 cells (spontaneously immortalized cell line) and colon cancer cell lines was detected using reverse transcription-quantitative PCR and western blotting. Cell Counting Kit-8 (CCK-8) and colony formation assays were used to assess cell viability and wound healing and Transwell assays were used to detect cell invasion and migration. ELISA was used to detect the expression levels of VEGF and tube formation assays were used to assess angiogenesis. The expression levels of angiogenesis-related proteins and AKT/ERK signaling pathway-related proteins were detected by western blotting. NR3C2 expression was downregulated in colon cancer cells and overexpression of NR3C2 inhibited proliferation, colony formation, migration and invasion of colon cancer cells. Overexpression of NR3C2 inhibited angiogenesis and activity of the AKT/ERK signaling pathway in colon cancer cells. Thus, it was demonstrated that NR3C2 inhibited the proliferation, colony formation, migration, invasion and angiogenesis of colon cancer cells through the AKT/ERK signaling pathway. These results may highlight novel targets for the treatment of colon cancer. D.A. Spandidos 2022-04 2022-02-18 /pmc/articles/PMC8908346/ /pubmed/35191517 http://dx.doi.org/10.3892/mmr.2022.12649 Text en Copyright: © Li et al. https://creativecommons.org/licenses/by-nc-nd/4.0/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, Jia Xu, Zhao NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title | NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title_full | NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title_fullStr | NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title_full_unstemmed | NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title_short | NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway |
title_sort | nr3c2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the akt/erk signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908346/ https://www.ncbi.nlm.nih.gov/pubmed/35191517 http://dx.doi.org/10.3892/mmr.2022.12649 |
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