Short-Term Hyperthermia Promotes the Sensitivity of MCF-7 Human Breast Cancer Cells to Paclitaxel

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  • Lin Yan
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Liu Zhihui
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Li Yongqiang
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Liao Xiaoli
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Liao Sina
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Cen Shaofang
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Yang Ling
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University
  • Wei Jiazhang
    Department of Clinical Pharmacology and Therapeutics, School of Medicine, Hamamatsu University
  • Hu Xiaohua
    Department of First Chemotherapy, Affiliated Cancer Hospital of Guangxi Medical University

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As a physical adjuvant approach in the treatment of solid tumors, regional hyperthermia plays a synergistic role in enhancing the efficacy of simultaneous chemotherapy. Paclitaxel (PTX) is an anti-mitotic taxane drug that is widely used in chemotherapy for the treatment of various human malignancies such as lung, ovarian, breast, and head and neck cancers. Since the possibility that hyperthermia can enhance the anti-tumor effects of PTX has not yet been investigated, the present study was designed to evaluate the effects of short-term hyperthermia on PTX-induced antitumor activity in the human breast cancer line MCF-7. It was found that short-term hyperthermia promoted PTX-induced suppression of cell proliferation. The IC50 for PTX was reduced from 18.2±1.0 to 15.0±0.45 nM (p<0.05). The level of PTX-induced cell apoptosis was increased from 8.5±1.2 to 16.4±2.4% (p<0.05) and from 15.2±1.4 to 34.9±2.8% (p<0.05), at the end of the first and second hyperthermia cycles, respectively; both the activity and expression of caspase-7 were enhanced. In addition, PTX-induced cell cycle arrest in the G2/M phase was further promoted by short-term hyperthermia, from 9.3±0.7 to 12.5±0.9% (p<0.05). In contrast, short-term hyperthermia affected neither tumor cell migration nor invasion in the presence or absence of PTX. The presented data thus suggest that short-term hyperthermia may serve as a feasible approach in the promotion of breast cancer cell sensitivity to PTX.

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