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YEATS2的过表达通过PI3K/AKT途径重塑细胞外基质以促进肝细胞癌进展。

Overexpression of YEATS2 Remodels the Extracellular Matrix to Promote Hepatocellular Carcinoma Progression via the PI3K/AKT Pathway.

作者信息

Liu Xin, Hu Yi, Li Cairong, Chen Jiayu, Liu Xiaohong, Shen Yang, Xu Yangtao, Chen Wenliang, Xu Ximing

机构信息

Department of Oncology, Renmin Hospital of Wuhan University, Wuhan 430060, China.

Department of Oncology, General Hospital of Central Theater Command, Wuhan 430061, China.

出版信息

Cancers (Basel). 2023 Mar 20;15(6):1850. doi: 10.3390/cancers15061850.

DOI:10.3390/cancers15061850
PMID:36980736
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10046954/
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.

摘要

肝细胞癌(HCC)是最常见的癌症之一,也是男性第四大死因。含YEATS结构域2(YEATS2)基因编码ATAC复合物的一个支架亚基。我们发现YEATS2在HCC组织中上调,且与预后不良相关。然而,YEATS2在HCC中的作用仍不清楚。本研究的目的是探讨YEATS2对HCC进展的影响并阐明其相关机制。我们发现YEATS2的过表达通过PI3K/AKT信号通路和细胞外基质调节促进肿瘤细胞增殖、迁移和侵袭。这些发现有助于理解YEATS2在HCC中的作用,并且YEATS2可能成为HCC治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/ac56a81931bc/cancers-15-01850-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/44ef91d3dad7/cancers-15-01850-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/0186bc62c8aa/cancers-15-01850-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/c8302457cdc6/cancers-15-01850-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/c484675ec040/cancers-15-01850-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/4ff144783cb9/cancers-15-01850-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/9aad137c20fe/cancers-15-01850-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/ac56a81931bc/cancers-15-01850-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/44ef91d3dad7/cancers-15-01850-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/0186bc62c8aa/cancers-15-01850-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/c8302457cdc6/cancers-15-01850-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/c484675ec040/cancers-15-01850-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/4ff144783cb9/cancers-15-01850-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/9aad137c20fe/cancers-15-01850-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ab/10046954/ac56a81931bc/cancers-15-01850-g007.jpg

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