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KAT6B May Be Applied as a Potential Therapeutic Target for Glioma

Glioma is a prevalent malignancy among brain tumors with high modality and low prognosis. Ferroptosis has been identified to play a crucial role in the progression and treatment of cancers. KAT6B, as a histone acetyltransferase, is involved in multiple cancer development. However, the function of KA...

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Autores principales: Liu, Yingzi, Duan, Xiaoyang, Zhang, Chunyan, Yuan, Jiangwei, Wen, Junpeng, Zheng, Cuihong, Shi, Jian, Yuan, Meng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007634/
https://www.ncbi.nlm.nih.gov/pubmed/35432536
http://dx.doi.org/10.1155/2022/2500092
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author Liu, Yingzi
Duan, Xiaoyang
Zhang, Chunyan
Yuan, Jiangwei
Wen, Junpeng
Zheng, Cuihong
Shi, Jian
Yuan, Meng
author_facet Liu, Yingzi
Duan, Xiaoyang
Zhang, Chunyan
Yuan, Jiangwei
Wen, Junpeng
Zheng, Cuihong
Shi, Jian
Yuan, Meng
author_sort Liu, Yingzi
collection PubMed
description Glioma is a prevalent malignancy among brain tumors with high modality and low prognosis. Ferroptosis has been identified to play a crucial role in the progression and treatment of cancers. KAT6B, as a histone acetyltransferase, is involved in multiple cancer development. However, the function of KAT6B in glioma is still elusive. Here, we aimed to evaluate the effect of KAT6B on ferroptosis in glioma cells and explored the potential mechanisms. We observed that the expression of KAT6B was enhanced in clinical glioma samples. The viability of glioma cells was repressed by erastin and the overexpression of KAT6B rescued the phenotype in the cells. Meanwhile, the apoptosis of glioma cells was induced by the treatment of erastin, while the overexpression of KAT6B blocked the effect in the cells. The levels of lipid ROS and iron were promoted by the treatment of erastin and the overexpression of KAT6B could reverse the effect in the cells. Mechanically, we identified that the expression of STAT3 was repressed by the KAT6B knockdown in glioma cells. The KAT6B was able to enrich on the promoter of STAT3 in glioma cells. Meanwhile, ChIP assay showed that the knockdown of KAT6B inhibited the enrichment of histone H3 lysine 23 acetylation (H3K23ac) and RNA polymerase II (RNA pol II) on STAT3 promoter in the cells. Depletion of STAT3 reversed KAT6B-regulated viability, apoptosis, and ferroptosis of glioma cells. Thus, we concluded that KAT6B contributes to glioma progression by repressing ferroptosis via epigenetically inducing STAT3.
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spelling pubmed-90076342022-04-14 KAT6B May Be Applied as a Potential Therapeutic Target for Glioma Liu, Yingzi Duan, Xiaoyang Zhang, Chunyan Yuan, Jiangwei Wen, Junpeng Zheng, Cuihong Shi, Jian Yuan, Meng J Oncol Research Article Glioma is a prevalent malignancy among brain tumors with high modality and low prognosis. Ferroptosis has been identified to play a crucial role in the progression and treatment of cancers. KAT6B, as a histone acetyltransferase, is involved in multiple cancer development. However, the function of KAT6B in glioma is still elusive. Here, we aimed to evaluate the effect of KAT6B on ferroptosis in glioma cells and explored the potential mechanisms. We observed that the expression of KAT6B was enhanced in clinical glioma samples. The viability of glioma cells was repressed by erastin and the overexpression of KAT6B rescued the phenotype in the cells. Meanwhile, the apoptosis of glioma cells was induced by the treatment of erastin, while the overexpression of KAT6B blocked the effect in the cells. The levels of lipid ROS and iron were promoted by the treatment of erastin and the overexpression of KAT6B could reverse the effect in the cells. Mechanically, we identified that the expression of STAT3 was repressed by the KAT6B knockdown in glioma cells. The KAT6B was able to enrich on the promoter of STAT3 in glioma cells. Meanwhile, ChIP assay showed that the knockdown of KAT6B inhibited the enrichment of histone H3 lysine 23 acetylation (H3K23ac) and RNA polymerase II (RNA pol II) on STAT3 promoter in the cells. Depletion of STAT3 reversed KAT6B-regulated viability, apoptosis, and ferroptosis of glioma cells. Thus, we concluded that KAT6B contributes to glioma progression by repressing ferroptosis via epigenetically inducing STAT3. Hindawi 2022-04-06 /pmc/articles/PMC9007634/ /pubmed/35432536 http://dx.doi.org/10.1155/2022/2500092 Text en Copyright © 2022 Yingzi Liu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liu, Yingzi
Duan, Xiaoyang
Zhang, Chunyan
Yuan, Jiangwei
Wen, Junpeng
Zheng, Cuihong
Shi, Jian
Yuan, Meng
KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title_full KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title_fullStr KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title_full_unstemmed KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title_short KAT6B May Be Applied as a Potential Therapeutic Target for Glioma
title_sort kat6b may be applied as a potential therapeutic target for glioma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007634/
https://www.ncbi.nlm.nih.gov/pubmed/35432536
http://dx.doi.org/10.1155/2022/2500092
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