HAUS1-mediated activation of CDK4 transcription enhances proliferation, invasion and migration in hepatocellular carcinoma.

IF 5 3区 医学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Lei Tang, Jun Zhao, Rongyuan Liang, Jiale Yang, Caiwei Chen, Zhonghuo Chen, Xiaofei Tao, Jianwei Yi, Taozhi Yu, Kai Wang
{"title":"HAUS1-mediated activation of CDK4 transcription enhances proliferation, invasion and migration in hepatocellular carcinoma.","authors":"Lei Tang, Jun Zhao, Rongyuan Liang, Jiale Yang, Caiwei Chen, Zhonghuo Chen, Xiaofei Tao, Jianwei Yi, Taozhi Yu, Kai Wang","doi":"10.1038/s41417-026-01014-x","DOIUrl":null,"url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is distinguished by aggressive proliferation, invasion, and migration, with its underlying molecular mechanisms remaining largely elusive.This study delves into the molecular mechanisms underlying HAUS1's role in HCC progression, focusing on its regulatory relationship with Cyclin-Dependent Kinase 4 (CDK4). We analyzed 34 HCC tissue specimens and conducted in vitro assays to evaluate HAUS1's impact on cell proliferation, invasion, migration, cycle and apoptosis. Potential molecules regulated by HAUS1 that could influence HCC function were further screened. Notably, HAUS1 was shown to activate CDK4 (Cyclin-Dependent Kinase 4) transcription, establishing a regulatory nexus where HAUS1-induced CDK4 expression exacerbates HCC malignancy. In vivo studies reinforced these findings, evidencing that HAUS1 influences tumor growth in xenograft models. Collectively, our research elucidates HAUS1's oncogenic role in HCC, mediated through CDK4 activation, and highlights its potential as a therapeutic target in HCC therapy. Mechanistic diagram illustrating how HAUS1 activates CDK4 transcription to promote proliferation, invasion and migration in HCC.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer gene therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41417-026-01014-x","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Hepatocellular carcinoma (HCC) is distinguished by aggressive proliferation, invasion, and migration, with its underlying molecular mechanisms remaining largely elusive.This study delves into the molecular mechanisms underlying HAUS1's role in HCC progression, focusing on its regulatory relationship with Cyclin-Dependent Kinase 4 (CDK4). We analyzed 34 HCC tissue specimens and conducted in vitro assays to evaluate HAUS1's impact on cell proliferation, invasion, migration, cycle and apoptosis. Potential molecules regulated by HAUS1 that could influence HCC function were further screened. Notably, HAUS1 was shown to activate CDK4 (Cyclin-Dependent Kinase 4) transcription, establishing a regulatory nexus where HAUS1-induced CDK4 expression exacerbates HCC malignancy. In vivo studies reinforced these findings, evidencing that HAUS1 influences tumor growth in xenograft models. Collectively, our research elucidates HAUS1's oncogenic role in HCC, mediated through CDK4 activation, and highlights its potential as a therapeutic target in HCC therapy. Mechanistic diagram illustrating how HAUS1 activates CDK4 transcription to promote proliferation, invasion and migration in HCC.

haus1介导的CDK4转录激活促进肝细胞癌的增殖、侵袭和迁移。
肝细胞癌(HCC)以侵袭性增殖、侵袭和迁移为特征,其潜在的分子机制在很大程度上尚不清楚。本研究深入研究了HAUS1在HCC进展中作用的分子机制,重点研究了其与细胞周期蛋白依赖性激酶4 (CDK4)的调节关系。我们分析了34例HCC组织标本,并通过体外实验来评估HAUS1对细胞增殖、侵袭、迁移、周期和凋亡的影响。进一步筛选HAUS1调控的可能影响HCC功能的分子。值得注意的是,HAUS1被证明可以激活CDK4(细胞周期蛋白依赖性激酶4)的转录,建立了一个调节关系,其中HAUS1诱导的CDK4表达加剧了HCC恶性肿瘤。体内研究强化了这些发现,证明HAUS1影响异种移植模型中的肿瘤生长。总的来说,我们的研究阐明了HAUS1在HCC中的致癌作用,通过CDK4激活介导,并强调了其作为HCC治疗靶点的潜力。说明HAUS1激活CDK4转录促进HCC增殖、侵袭和迁移的机制图。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Cancer gene therapy
Cancer gene therapy 医学-生物工程与应用微生物
CiteScore
10.20
自引率
0.00%
发文量
150
审稿时长
4-8 weeks
期刊介绍: Cancer Gene Therapy is the essential gene and cellular therapy resource for cancer researchers and clinicians, keeping readers up to date with the latest developments in gene and cellular therapies for cancer. The journal publishes original laboratory and clinical research papers, case reports and review articles. Publication topics include RNAi approaches, drug resistance, hematopoietic progenitor cell gene transfer, cancer stem cells, cellular therapies, homologous recombination, ribozyme technology, antisense technology, tumor immunotherapy and tumor suppressors, translational research, cancer therapy, gene delivery systems (viral and non-viral), anti-gene therapy (antisense, siRNA & ribozymes), apoptosis; mechanisms and therapies, vaccine development, immunology and immunotherapy, DNA synthesis and repair. Cancer Gene Therapy publishes the results of laboratory investigations, preclinical studies, and clinical trials in the field of gene transfer/gene therapy and cellular therapies as applied to cancer research. Types of articles published include original research articles; case reports; brief communications; review articles in the main fields of drug resistance/sensitivity, gene therapy, cellular therapy, tumor suppressor and anti-oncogene therapy, cytokine/tumor immunotherapy, etc.; industry perspectives; and letters to the editor.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书