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Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway
SIMPLE SUMMARY: Hepatocellular carcinoma (HCC) is a malignant tumor with a high incidence rate and the fourth leading cause of death in cancer patients. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046954/ https://www.ncbi.nlm.nih.gov/pubmed/36980736 http://dx.doi.org/10.3390/cancers15061850 |
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author | Liu, Xin Hu, Yi Li, Cairong Chen, Jiayu Liu, Xiaohong Shen, Yang Xu, Yangtao Chen, Wenliang Xu, Ximing |
author_facet | Liu, Xin Hu, Yi Li, Cairong Chen, Jiayu Liu, Xiaohong Shen, Yang Xu, Yangtao Chen, Wenliang Xu, Ximing |
author_sort | Liu, Xin |
collection | PubMed |
description | SIMPLE SUMMARY: Hepatocellular carcinoma (HCC) is a malignant tumor with a high incidence rate and the fourth leading cause of death in cancer patients. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and was associated with poorer prognosis of patients. We found that overexpression of YEATS2 promoted the process of tumor proliferation, migration, and invasion. Mechanistically, we revealed that YEATS2 promoted liver cancer progression by activating the PI3K/AKT signaling pathway and remodeling the extracellular matrix. Therefore, these findings suggest that YEATS2 holds promise as a new therapeutic target. ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most common cancers and the fourth leading cause of death in men. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and was associated with a poor prognosis. However, the role of YEATS2 in HCC remains unclear. The purpose of this study was to investigate the effect of YEATS2 on the progression of HCC and to elucidate its related mechanisms. We found that overexpression of YEATS2 promoted tumor cell proliferation, migration, and invasion through the PI3K/AKT signaling pathway and regulation of extracellular matrix. These findings help to understand the role of YEATS2 in HCC, and YEATS2 may become a new target for HCC therapy. |
format | Online Article Text |
id | pubmed-10046954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-100469542023-03-29 Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway Liu, Xin Hu, Yi Li, Cairong Chen, Jiayu Liu, Xiaohong Shen, Yang Xu, Yangtao Chen, Wenliang Xu, Ximing Cancers (Basel) Article SIMPLE SUMMARY: Hepatocellular carcinoma (HCC) is a malignant tumor with a high incidence rate and the fourth leading cause of death in cancer patients. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and was associated with poorer prognosis of patients. We found that overexpression of YEATS2 promoted the process of tumor proliferation, migration, and invasion. Mechanistically, we revealed that YEATS2 promoted liver cancer progression by activating the PI3K/AKT signaling pathway and remodeling the extracellular matrix. Therefore, these findings suggest that YEATS2 holds promise as a new therapeutic target. ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most common cancers and the fourth leading cause of death in men. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and was associated with a poor prognosis. However, the role of YEATS2 in HCC remains unclear. The purpose of this study was to investigate the effect of YEATS2 on the progression of HCC and to elucidate its related mechanisms. We found that overexpression of YEATS2 promoted tumor cell proliferation, migration, and invasion through the PI3K/AKT signaling pathway and regulation of extracellular matrix. These findings help to understand the role of YEATS2 in HCC, and YEATS2 may become a new target for HCC therapy. MDPI 2023-03-20 /pmc/articles/PMC10046954/ /pubmed/36980736 http://dx.doi.org/10.3390/cancers15061850 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Liu, Xin Hu, Yi Li, Cairong Chen, Jiayu Liu, Xiaohong Shen, Yang Xu, Yangtao Chen, Wenliang Xu, Ximing Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title | Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title_full | Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title_fullStr | Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title_full_unstemmed | Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title_short | Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway |
title_sort | overexpression of yeats2 remodels the extracellular matrix to promote hepatocellular carcinoma progression via the pi3k/akt pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046954/ https://www.ncbi.nlm.nih.gov/pubmed/36980736 http://dx.doi.org/10.3390/cancers15061850 |
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