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FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma

FOXA1 is associated with malignant tumors, but the function of FOXA1 in EOC is unclear. HDAC3 can influence the proliferation, migration and invasion ability of EOC. In this study, we wanted to explore the function of FOXA1 in ovarian cancer and the relationship between HDAC3 and FOXA1.The expressio...

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Autores principales: Lou, Tong, Liu, Chongdong, Qu, Hong, Zhang, Zhiqiang, Wang, Shuzhen, Zhuang, Huiyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8740004/
https://www.ncbi.nlm.nih.gov/pubmed/34991620
http://dx.doi.org/10.1186/s12967-021-03224-3
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author Lou, Tong
Liu, Chongdong
Qu, Hong
Zhang, Zhiqiang
Wang, Shuzhen
Zhuang, Huiyu
author_facet Lou, Tong
Liu, Chongdong
Qu, Hong
Zhang, Zhiqiang
Wang, Shuzhen
Zhuang, Huiyu
author_sort Lou, Tong
collection PubMed
description FOXA1 is associated with malignant tumors, but the function of FOXA1 in EOC is unclear. HDAC3 can influence the proliferation, migration and invasion ability of EOC. In this study, we wanted to explore the function of FOXA1 in ovarian cancer and the relationship between HDAC3 and FOXA1.The expression of HDAC3 and FOXA1 was detected by immunohistochemical staining of primary lesions from 127 epithelial ovarian carcinoma patients. A proliferation assay, a Transwell assay, an apoptosis assay and animal experiments were used to assess the proliferation, invasion and apoptosis abilities of ovarian cancer cells before and after transfection with FOXA1. The relevance of the in vitro findings was confirmed in xenografts. The H-scores for FOXA1 and HDAC3 staining in FIGO stage III-IV were noticeably higher and predicted adverse clinical outcomes in patients with ovarian cancer. The expression level of HDAC3 was significantly correlated with the expression level of FOXA1. Invasion, proliferation and apoptosis capacity and tumor formation were decreased in the FOXA1-knockdown cells. Experiments in xenografts confirmed that HDAC3 mediated tumor formation. In conclusion, FOXA1 can be modulated by HDAC3 through the Wnt/β-catenin signaling pathway, and FOXA1 plays essential roles in the proliferation, apoptosis and invasion of EOC cell lines and xenograft experiments.
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spelling pubmed-87400042022-01-07 FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma Lou, Tong Liu, Chongdong Qu, Hong Zhang, Zhiqiang Wang, Shuzhen Zhuang, Huiyu J Transl Med Research FOXA1 is associated with malignant tumors, but the function of FOXA1 in EOC is unclear. HDAC3 can influence the proliferation, migration and invasion ability of EOC. In this study, we wanted to explore the function of FOXA1 in ovarian cancer and the relationship between HDAC3 and FOXA1.The expression of HDAC3 and FOXA1 was detected by immunohistochemical staining of primary lesions from 127 epithelial ovarian carcinoma patients. A proliferation assay, a Transwell assay, an apoptosis assay and animal experiments were used to assess the proliferation, invasion and apoptosis abilities of ovarian cancer cells before and after transfection with FOXA1. The relevance of the in vitro findings was confirmed in xenografts. The H-scores for FOXA1 and HDAC3 staining in FIGO stage III-IV were noticeably higher and predicted adverse clinical outcomes in patients with ovarian cancer. The expression level of HDAC3 was significantly correlated with the expression level of FOXA1. Invasion, proliferation and apoptosis capacity and tumor formation were decreased in the FOXA1-knockdown cells. Experiments in xenografts confirmed that HDAC3 mediated tumor formation. In conclusion, FOXA1 can be modulated by HDAC3 through the Wnt/β-catenin signaling pathway, and FOXA1 plays essential roles in the proliferation, apoptosis and invasion of EOC cell lines and xenograft experiments. BioMed Central 2022-01-06 /pmc/articles/PMC8740004/ /pubmed/34991620 http://dx.doi.org/10.1186/s12967-021-03224-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Lou, Tong
Liu, Chongdong
Qu, Hong
Zhang, Zhiqiang
Wang, Shuzhen
Zhuang, Huiyu
FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title_full FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title_fullStr FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title_full_unstemmed FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title_short FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma
title_sort foxa1 can be modulated by hdac3 in the progression of epithelial ovarian carcinoma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8740004/
https://www.ncbi.nlm.nih.gov/pubmed/34991620
http://dx.doi.org/10.1186/s12967-021-03224-3
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