Scholarlink

<p>Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, with treatment failure often attributed to chemoresistance and evasion of apoptosis. Cathayanon E (CE), a natural chalcone derivative isolated from Morus alba, has shown anticancer potential, but its role and mechanism in CRC remain largely unexplored. In this study, CE significantly inhibited CRC cell proliferation and induced apoptosis both in vitro and in vivo. Mechanistically, CE directly bound to the anti-apoptotic protein MCL1 and promoted its β-TRCP–mediated ubiquitination and proteasomal degradation, thereby inducing mitochondrial apoptotic signaling. Overexpression of MCL1 reversed the antiproliferative and pro-apoptotic effects of CE, validating MCL1 as a functional target of CE. Furthermore, CE markedly enhanced the chemosensitivity of CRC cells to oxaliplatin, resulting in synergistic tumor suppression in xenograft models. These findings highlight CE as a promising natural agent that targets MCL1 to overcome chemoresistance and improve therapeutic outcomes in colorectal cancer.</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

Cathayanon E induces apoptosis and enhances oxaliplatin sensitivity in colorectal cancer through suppression of MCL1

  • 期刊论文

  • 发表日期：

    2025年9月9日

查看全文
  • Liang Cen,
  • Xin Hu,
  • Guozhen An,
  • Lichao Wang,
  • Yanghao Hu,
  • Junjie He,
  • Hanghang Qin,
  • Yongsen Li,
  • Hongjuan Cui

摘要

Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, with treatment failure often attributed to chemoresistance and evasion of apoptosis. Cathayanon E (CE), a natural chalcone derivative isolated from Morus alba, has shown anticancer potential, but its role and mechanism in CRC remain largely unexplored. In this study, CE significantly inhibited CRC cell proliferation and induced apoptosis both in vitro and in vivo. Mechanistically, CE directly bound to the anti-apoptotic protein MCL1 and promoted its β-TRCP–mediated ubiquitination and proteasomal degradation, thereby inducing mitochondrial apoptotic signaling. Overexpression of MCL1 reversed the antiproliferative and pro-apoptotic effects of CE, validating MCL1 as a functional target of CE. Furthermore, CE markedly enhanced the chemosensitivity of CRC cells to oxaliplatin, resulting in synergistic tumor suppression in xenograft models. These findings highlight CE as a promising natural agent that targets MCL1 to overcome chemoresistance and improve therapeutic outcomes in colorectal cancer.