miR-520b Inhibits IGF-1R to Increase Doxorubicin Sensitivity and Promote Cell Apoptosis in Breast Cancer

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  • Zhang Hui
    Breast Cancer Center, Chongqing University Cancer Hospital and Chongqing Cancer Institute and Chongqing Cancer Hospital
  • Zheng Xiao-Dong
    Breast Cancer Center, Chongqing University Cancer Hospital and Chongqing Cancer Institute and Chongqing Cancer Hospital
  • Zeng Xiao-Hua
    Breast Cancer Center, Chongqing University Cancer Hospital and Chongqing Cancer Institute and Chongqing Cancer Hospital
  • Li Li
    Department of Gynecologic Oncology, Affiliated Tumor Hospital of Guangxi Medical University
  • Zhou Qi
    Department of Gynecologic Oncology, Chongqing University Cancer Hospital and Chongqing Cancer Institute and Chongqing Cancer Hospital Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital and Chongqing Cancer Institute and Chongqing Cancer Hospital

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<p>Doxorubicin (DOX) is currently one of the most widely used and effective drugs for the treatment of breast cancer, but drug resistance in breast cancer often leads to poor efficacy. MicroRNAs (miRNAs) are involved in the development and progression of various tumors and increasing number of studies have confirmed that abnormal miR-520b expression is closely associated breast cancer. We analyzed the clinical features, including miR-520b, of 30 patients with breast cancer. Further, we analyzed the interaction between miR-520b and insulin-like growth factor 1 receptor (IGF-1R) in breast cancer cell. miR-520b expression was significantly increased in chemotherapy-sensitive patients and was positively correlated with the chemotherapeutic efficacy in breast cancer. Cell proliferation assay confirmed that miR-520b promotes DOX-induced breast cancer cell apoptosis by regulating the PI3K/AKT signaling pathway. Moreover, bioinformatics method and dual luciferase reporter assay demonstrated that miR-520b negatively regulates IGF-1R, and IGF-1R overexpression and enhanced activity are closely associated with tumor development, progression, metastasis, and chemotherapy resistance. Similarly, cell proliferation assay showed that IGF-1R is negatively correlated with the efficacy of DOX chemotherapy and affects cell apoptosis mediated by the PI3K/AKT signaling pathway. On the contrary, miR-520b can downregulate the expression of IGF-1R. miR-520b increases DOX sensitivity and promotes cell apoptosis in breast cancer by inhibiting IGF-1R expression by the PI3K/AKT signaling pathway.</p>

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  • 薬学雑誌

    薬学雑誌 141 (3), 415-426, 2021-03-01

    公益社団法人 日本薬学会

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