Scholarlink

<p>Oral squamous cell carcinoma (OSCC) is a prevalent and aggressive malignancy of the oral cavity, with increasing incidence and poor prognosis. Myeloid leukemia 1 (Mcl-1), an anti-apoptotic protein in the BCL-2 family, is critical for tumor development and progression. In this study, we investigated Dioscin, a natural compound, as a potential therapeutic agent for OSCC. Our results demonstrated that Dioscin significantly inhibits cell viability and colony formation in OSCC cell lines. Mechanistically, Dioscin induced intrinsic apoptosis by promoting the ubiquitination and degradation of Mcl-1. Further analysis revealed that Dioscin enhances the interaction between the E3 ligase β-TRCP and Mcl-1 by inhibiting the Akt/GSK3β signaling pathway, resulting in increased phosphorylation of Mcl-1 at Ser159, which drives its destabilization. In vivo, Dioscin notably suppressed OSCC tumor growth, including in sensitive and radioresistant cells, by reducing Mcl-1 levels. These findings highlight the therapeutic potential of Dioscin for OSCC treatment, offering new insights for overcoming radioresistance and improving clinical outcomes in OSCC patients.</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

Dioscin suppresses tumorigenesis and overcomes radioresistance by promoting ubiquitination-mediated degradation of Mcl-1

  • 期刊论文

  • 发表日期：

    2026年3月24日

查看全文
  • Qi Liang,
  • Xuecheng Wu,
  • Dongyu Li,
  • Yiwei Liu,
  • Ruirui Wang,
  • Xiaoying Li,
  • Pengfei Guo,
  • Wei Li

摘要

Oral squamous cell carcinoma (OSCC) is a prevalent and aggressive malignancy of the oral cavity, with increasing incidence and poor prognosis. Myeloid leukemia 1 (Mcl-1), an anti-apoptotic protein in the BCL-2 family, is critical for tumor development and progression. In this study, we investigated Dioscin, a natural compound, as a potential therapeutic agent for OSCC. Our results demonstrated that Dioscin significantly inhibits cell viability and colony formation in OSCC cell lines. Mechanistically, Dioscin induced intrinsic apoptosis by promoting the ubiquitination and degradation of Mcl-1. Further analysis revealed that Dioscin enhances the interaction between the E3 ligase β-TRCP and Mcl-1 by inhibiting the Akt/GSK3β signaling pathway, resulting in increased phosphorylation of Mcl-1 at Ser159, which drives its destabilization. In vivo, Dioscin notably suppressed OSCC tumor growth, including in sensitive and radioresistant cells, by reducing Mcl-1 levels. These findings highlight the therapeutic potential of Dioscin for OSCC treatment, offering new insights for overcoming radioresistance and improving clinical outcomes in OSCC patients.