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HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells

Choroidal melanoma (CM) is the most common type of diagnosed uveal melanoma (UM), which is prone to metastasis and exhibits a poor prognosis. The molecular mechanisms underlying CM progression need further elucidation to research effective therapeutic strategies. Histone deacetylase 7 (HDAC7) is ver...

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Autores principales: Zhang, Yimeng, Ding, Peng, Wang, Yuanyong, Shao, Changjian, Guo, Kai, Yang, Hanyi, Feng, Yingtong, Ning, Jiayi, Pan, Minghong, Wang, Ping, Yan, Xiaolong, Ma, Zhiqiang, Han, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9849404/
https://www.ncbi.nlm.nih.gov/pubmed/36653340
http://dx.doi.org/10.1038/s41419-022-05522-0
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author Zhang, Yimeng
Ding, Peng
Wang, Yuanyong
Shao, Changjian
Guo, Kai
Yang, Hanyi
Feng, Yingtong
Ning, Jiayi
Pan, Minghong
Wang, Ping
Yan, Xiaolong
Ma, Zhiqiang
Han, Jing
author_facet Zhang, Yimeng
Ding, Peng
Wang, Yuanyong
Shao, Changjian
Guo, Kai
Yang, Hanyi
Feng, Yingtong
Ning, Jiayi
Pan, Minghong
Wang, Ping
Yan, Xiaolong
Ma, Zhiqiang
Han, Jing
author_sort Zhang, Yimeng
collection PubMed
description Choroidal melanoma (CM) is the most common type of diagnosed uveal melanoma (UM), which is prone to metastasis and exhibits a poor prognosis. The molecular mechanisms underlying CM progression need further elucidation to research effective therapeutic strategies. Histone deacetylase 7 (HDAC7) is very important in regulating cancer progression, but the significance and effect of HDAC7 on CM progression are unclear. In the present study, we found that HDAC7 is overexpressed in CM tissues versus normal tissues. We built HDAC7 overexpressing CM cell lines to study the functions of HDAC7 in CM progression and verified that upregulation of HDAC7 promoted the proliferation and metastasis of CM cells, while pharmacological inhibition of HDAC7 suppressed both the proliferation and metastasis of CM cells. Furthermore, we found that the aforementioned cancer-promoting effect of HDAC7 was mediated by c-Myc. Targeted inhibition of c-Myc inhibited CM progression by interfering with the HDAC7/c-Myc signaling pathway. Our study highlighted the function of targeting the HDAC7/c-Myc signaling pathway to intervene in the pathological process of CM, which provides potential therapeutic strategies for CM treatment.
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spelling pubmed-98494042023-01-20 HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells Zhang, Yimeng Ding, Peng Wang, Yuanyong Shao, Changjian Guo, Kai Yang, Hanyi Feng, Yingtong Ning, Jiayi Pan, Minghong Wang, Ping Yan, Xiaolong Ma, Zhiqiang Han, Jing Cell Death Dis Article Choroidal melanoma (CM) is the most common type of diagnosed uveal melanoma (UM), which is prone to metastasis and exhibits a poor prognosis. The molecular mechanisms underlying CM progression need further elucidation to research effective therapeutic strategies. Histone deacetylase 7 (HDAC7) is very important in regulating cancer progression, but the significance and effect of HDAC7 on CM progression are unclear. In the present study, we found that HDAC7 is overexpressed in CM tissues versus normal tissues. We built HDAC7 overexpressing CM cell lines to study the functions of HDAC7 in CM progression and verified that upregulation of HDAC7 promoted the proliferation and metastasis of CM cells, while pharmacological inhibition of HDAC7 suppressed both the proliferation and metastasis of CM cells. Furthermore, we found that the aforementioned cancer-promoting effect of HDAC7 was mediated by c-Myc. Targeted inhibition of c-Myc inhibited CM progression by interfering with the HDAC7/c-Myc signaling pathway. Our study highlighted the function of targeting the HDAC7/c-Myc signaling pathway to intervene in the pathological process of CM, which provides potential therapeutic strategies for CM treatment. Nature Publishing Group UK 2023-01-18 /pmc/articles/PMC9849404/ /pubmed/36653340 http://dx.doi.org/10.1038/s41419-022-05522-0 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Zhang, Yimeng
Ding, Peng
Wang, Yuanyong
Shao, Changjian
Guo, Kai
Yang, Hanyi
Feng, Yingtong
Ning, Jiayi
Pan, Minghong
Wang, Ping
Yan, Xiaolong
Ma, Zhiqiang
Han, Jing
HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title_full HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title_fullStr HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title_full_unstemmed HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title_short HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
title_sort hdac7/c-myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9849404/
https://www.ncbi.nlm.nih.gov/pubmed/36653340
http://dx.doi.org/10.1038/s41419-022-05522-0
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