Scholarlink

<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.</p><p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 发表日期：

    2026年3月6日

查看全文
  • Lei Tang,
  • Jun Zhao,
  • Rongyuan Liang,
  • Jiale Yang,
  • Caiwei Chen,
  • Zhonghuo Chen,
  • Xiaofei Tao,
  • Jianwei Yi,
  • Taozhi Yu,
  • Kai Wang

摘要

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.