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<p>The cell cycle is regulated by complex mechanisms that are essential for preventing and controlling tumorigenesis. CDK4/6 inhibitors are drugs that target cell cycle proteins and restore normal cell cycle progression. In breast cancer, CDK4/6 inhibitors can also block the distant metastasis of cancer cells. In this study, we used computer-aided drug design to identify a novel compound, WXJ-114, which has a high binding affinity for CDK4/6 and can potentially inhibit its activity. We evaluated the effects of WXJ-114 on breast cancer cells using various assays, such as MTT, wound healing, invasion, and colony formation. We found that WXJ-114 inhibited the adhesion, proliferation, migration, and invasion of breast cancer cells, induced apoptosis, and modulated the expression of proteins involved in the CDK4/6-cyclinD-Rb-E2F signaling pathway. We also tested the antitumor and antiangiogenic activity of WXJ-114 in a chicken embryo chorioallantoic membrane model, and observed that WXJ-114 significantly suppressed tumor growth and angiogenesis. These results suggest that WXJ-114 exhibits potent anti-breast cancer activity by interfering with the CDK4/6-cyclin D-Rb-E2F pathway, which provides a basis for further development of targeted therapies for breast cancer.</p>

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WXJ-114, A New CDK4/6 Inhibitor that Treats Breast Cancer by Blocking Cell Cycles

  • 期刊论文

  • 发表日期：

    2025年7月1日

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  • Jing Ji,
  • Jiaojiao Zhou,
  • Xiao Hou,
  • Luyao Zhang,
  • Lingyi Zuo,
  • Hanxue Li,
  • Meiqi Zhang,
  • Yuanyuan Liu,
  • Xing Liu,
  • Qilan Qian,
  • Jingting Qin,
  • Jinming Ma,
  • Menghan Xu,
  • Xiujun Wang,
  • Bin Liu

摘要

The cell cycle is regulated by complex mechanisms that are essential for preventing and controlling tumorigenesis. CDK4/6 inhibitors are drugs that target cell cycle proteins and restore normal cell cycle progression. In breast cancer, CDK4/6 inhibitors can also block the distant metastasis of cancer cells. In this study, we used computer-aided drug design to identify a novel compound, WXJ-114, which has a high binding affinity for CDK4/6 and can potentially inhibit its activity. We evaluated the effects of WXJ-114 on breast cancer cells using various assays, such as MTT, wound healing, invasion, and colony formation. We found that WXJ-114 inhibited the adhesion, proliferation, migration, and invasion of breast cancer cells, induced apoptosis, and modulated the expression of proteins involved in the CDK4/6-cyclinD-Rb-E2F signaling pathway. We also tested the antitumor and antiangiogenic activity of WXJ-114 in a chicken embryo chorioallantoic membrane model, and observed that WXJ-114 significantly suppressed tumor growth and angiogenesis. These results suggest that WXJ-114 exhibits potent anti-breast cancer activity by interfering with the CDK4/6-cyclin D-Rb-E2F pathway, which provides a basis for further development of targeted therapies for breast cancer.