Scholarlink

<p>The occurrence and death rates of colorectal cancer (CRC) have been consistently increasing, demanding the immediate requirement for the creation of dependable and effective medicinal treatments. This study investigates bardoxolone methyl (CDDO-Me), a synthetic triterpenoid, as a potential therapeutic agent for CRC. Integrating network pharmacology, bioinformatic analyses, and in vitro assays, we evaluated the effects of CDDO-Me on CRC cells. In vitro studies indicate that CDDO-Me significantly inhibits the growth of CRC cells, specifically HCT116 and RKO, with IC<sub>50</sub> values of 3.17 µM and 7.64 µM, respectively. Additionally, CDDO-Me effectively suppresses the PI3K signaling pathway and increases reactive oxygen species (ROS) levels in CRC cells. Consequently, this leads to G2/M phase arrest, an increase in apoptosis (over 30%), and a decrease in adhesion and invasion capabilities. Importantly, these effects were reversible upon the administration of N-acetylcysteine. Collectively, our findings provide compelling evidence for the potential of CDDO-Me as a promising candidate for the treatment of CRC.</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

Bardoxolone methyl suppressed colorectal cancer cells in vitro by inhibiting the PI3K signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月5日

查看全文
  • Linlin Zhang,
  • Qiaoling Huang,
  • Jingqing Yang,
  • Ye Hu

摘要

The occurrence and death rates of colorectal cancer (CRC) have been consistently increasing, demanding the immediate requirement for the creation of dependable and effective medicinal treatments. This study investigates bardoxolone methyl (CDDO-Me), a synthetic triterpenoid, as a potential therapeutic agent for CRC. Integrating network pharmacology, bioinformatic analyses, and in vitro assays, we evaluated the effects of CDDO-Me on CRC cells. In vitro studies indicate that CDDO-Me significantly inhibits the growth of CRC cells, specifically HCT116 and RKO, with IC50 values of 3.17 µM and 7.64 µM, respectively. Additionally, CDDO-Me effectively suppresses the PI3K signaling pathway and increases reactive oxygen species (ROS) levels in CRC cells. Consequently, this leads to G2/M phase arrest, an increase in apoptosis (over 30%), and a decrease in adhesion and invasion capabilities. Importantly, these effects were reversible upon the administration of N-acetylcysteine. Collectively, our findings provide compelling evidence for the potential of CDDO-Me as a promising candidate for the treatment of CRC.