ASIC1 promotes migration and invasion of hepatocellular carcinoma via the PRKACA/AP-1 signaling pathway.

IF 3.3 3区 医学 Q2 ONCOLOGY
Youyi Liu, Boshi Wang, Yang Cheng, Yipeng Fang, Yingjian Hou, Yong Mao, Xiaomin Wu, Donglin Jiang, Youzhao He, Cheng Jin
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引用次数: 0

Abstract

Hepatocellular carcinoma (HCC) exhibits a high mortality rate due to its high invasion and metastatic nature, and the acidic microenvironment plays a pivotal role. Acid-sensing ion channel 1 (ASIC1) is upregulated in HCC tissues and facilitates tumor progression in a pH-dependent manner, while the specific mechanisms therein remain currently unclear. Herein, we aimed to investigate the underlying mechanisms by which ASIC1 contributes to the development of HCC. Using bioinformatics analysis, we found a significant association between ASIC1 expression and malignant transformation of HCC, such as poor prognosis, metastasis and recurrence. Specifically, ASIC1 enhanced the migration and invasion capabilities of Li-7 cells in the in vivo experiment using an HCC lung metastasis mouse model, as well as in the in vitro experiments such as wound healing assay and Transwell assay. Furthermore, our comprehensive gene chip and molecular biology experiments revealed that ASIC1 promoted HCC migration and invasion by activating the PRKACA/AP-1 signaling pathway. Our findings indicate that targeting ASIC1 could have therapeutic potential for inhibiting HCC progression.

ASIC1 通过 PRKACA/AP-1 信号通路促进肝细胞癌的迁移和侵袭。
肝细胞癌(HCC)具有高侵袭性和高转移性,因此死亡率很高,而酸性微环境在其中起着举足轻重的作用。酸感应离子通道 1(ASIC1)在 HCC 组织中上调,并以 pH 依赖性方式促进肿瘤进展,但其中的具体机制目前仍不清楚。在此,我们旨在研究 ASIC1 促进 HCC 发展的潜在机制。通过生物信息学分析,我们发现 ASIC1 的表达与 HCC 的恶性转化(如预后不良、转移和复发)之间存在显著关联。具体来说,在 HCC 肺转移小鼠模型的体内实验中,以及在伤口愈合实验和 Transwell 实验等体外实验中,ASIC1 都增强了 Li-7 细胞的迁移和侵袭能力。此外,我们的基因芯片和分子生物学综合实验还发现,ASIC1 通过激活 PRKACA/AP-1 信号通路促进了 HCC 的迁移和侵袭。我们的研究结果表明,以ASIC1为靶点可能具有抑制HCC进展的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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