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Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression
The function of activating transcription factor 3 (ATF3) in cancer is context-dependent and its role in endometrial carcinoma (EC) is yet to be elucidated. In the present study, ATF3 was indicated to be downregulated, while one of the ATF3-interacting proteins, JunB, was upregulated in ECs according...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7384851/ https://www.ncbi.nlm.nih.gov/pubmed/32582999 http://dx.doi.org/10.3892/ijo.2020.5084 |
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author | Wang, Fangyuan Li, Jingjing Wang, Haixia Zhang, Fan Gao, Jin |
author_facet | Wang, Fangyuan Li, Jingjing Wang, Haixia Zhang, Fan Gao, Jin |
author_sort | Wang, Fangyuan |
collection | PubMed |
description | The function of activating transcription factor 3 (ATF3) in cancer is context-dependent and its role in endometrial carcinoma (EC) is yet to be elucidated. In the present study, ATF3 was indicated to be downregulated, while one of the ATF3-interacting proteins, JunB, was upregulated in ECs according to western blot analysis. After overexpression in ECs, ATF3 inhibited the proliferation and invasion of EC cells and enhanced apoptosis, as well as suppressed the expression of JunB. The properties of EC cells, including the expression of matrix metalloproteinases, tissue inhibitors of metallo-proteinases, the cell cycle and apoptosis were all altered by overexpression of ATF3. Furthermore, luciferase activity assay, chromatin precipitation and DNA affinity assay results indicated that ATF3 exerted the aforementioned functions via JunB binding and activator protein-1 signaling. However, the interaction between ATF3 and JunB did not occur in EC cells under basal conditions, but in ATF3-overexpressing ECs, which was capable of mitigating EC proliferation, invasion and metastasis. Collectively, the present results suggested that the ATF3/JunB interaction may serve as a potential therapeutic target for ECs. |
format | Online Article Text |
id | pubmed-7384851 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73848512020-07-30 Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression Wang, Fangyuan Li, Jingjing Wang, Haixia Zhang, Fan Gao, Jin Int J Oncol Articles The function of activating transcription factor 3 (ATF3) in cancer is context-dependent and its role in endometrial carcinoma (EC) is yet to be elucidated. In the present study, ATF3 was indicated to be downregulated, while one of the ATF3-interacting proteins, JunB, was upregulated in ECs according to western blot analysis. After overexpression in ECs, ATF3 inhibited the proliferation and invasion of EC cells and enhanced apoptosis, as well as suppressed the expression of JunB. The properties of EC cells, including the expression of matrix metalloproteinases, tissue inhibitors of metallo-proteinases, the cell cycle and apoptosis were all altered by overexpression of ATF3. Furthermore, luciferase activity assay, chromatin precipitation and DNA affinity assay results indicated that ATF3 exerted the aforementioned functions via JunB binding and activator protein-1 signaling. However, the interaction between ATF3 and JunB did not occur in EC cells under basal conditions, but in ATF3-overexpressing ECs, which was capable of mitigating EC proliferation, invasion and metastasis. Collectively, the present results suggested that the ATF3/JunB interaction may serve as a potential therapeutic target for ECs. D.A. Spandidos 2020-06-19 /pmc/articles/PMC7384851/ /pubmed/32582999 http://dx.doi.org/10.3892/ijo.2020.5084 Text en Copyright: © Wang 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 Wang, Fangyuan Li, Jingjing Wang, Haixia Zhang, Fan Gao, Jin Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title | Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title_full | Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title_fullStr | Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title_full_unstemmed | Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title_short | Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression |
title_sort | activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via junb suppression |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7384851/ https://www.ncbi.nlm.nih.gov/pubmed/32582999 http://dx.doi.org/10.3892/ijo.2020.5084 |
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