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    魏欣宇, 高鹏, 刘佳欣, 王文锐, 杨清玲, 陈昌杰. 紫杉醇耐药乳腺癌细胞外泌体来源的miR-5585-5p诱导乳腺癌细胞产生耐药表型研究[J]. 蚌埠医科大学学报, 2021, 46(8): 989-993. DOI: 10.13898/j.cnki.issn.1000-2200.2021.08.001
    引用本文: 魏欣宇, 高鹏, 刘佳欣, 王文锐, 杨清玲, 陈昌杰. 紫杉醇耐药乳腺癌细胞外泌体来源的miR-5585-5p诱导乳腺癌细胞产生耐药表型研究[J]. 蚌埠医科大学学报, 2021, 46(8): 989-993. DOI: 10.13898/j.cnki.issn.1000-2200.2021.08.001
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    WEI Xin-yu, GAO Peng, LIU Jia-xin, WANG Wen-rui, YANG Qing-ling, CHEN Chang-jie. Study on the drug-resistant phenotypes of breast cancer cells induced by exosomal miR-5585-5p derived from paclitaxel-resistant breast cancer cells[J]. Journal of Bengbu Medical University, 2021, 46(8): 989-993. DOI: 10.13898/j.cnki.issn.1000-2200.2021.08.001
    Citation: WEI Xin-yu, GAO Peng, LIU Jia-xin, WANG Wen-rui, YANG Qing-ling, CHEN Chang-jie. Study on the drug-resistant phenotypes of breast cancer cells induced by exosomal miR-5585-5p derived from paclitaxel-resistant breast cancer cells[J]. Journal of Bengbu Medical University, 2021, 46(8): 989-993. DOI: 10.13898/j.cnki.issn.1000-2200.2021.08.001
    shu

    紫杉醇耐药乳腺癌细胞外泌体来源的miR-5585-5p诱导乳腺癌细胞产生耐药表型研究

    Study on the drug-resistant phenotypes of breast cancer cells induced by exosomal miR-5585-5p derived from paclitaxel-resistant breast cancer cells

      摘要
    • 摘要:
      目的研究紫杉醇耐药乳腺癌细胞外泌体来源的miR-5585-5p对乳腺癌细胞迁移、凋亡和耐药性的影响。
      方法超速离心法获取外泌体，使用qRT-PCR方法分别检测乳腺癌细胞（SKBR-3）和紫杉醇耐药乳腺癌细胞（SKBR-3/PR）细胞株和外泌体中miR-5585-5p的表达量；通过外泌体共培养技术以及在乳腺癌耐药细胞中转染miR-5585-5p的抑制剂，用Transwell检测其迁移能力，流式细胞术检测其凋亡情况；qRT-PCR和Western blotting检测其耐药指标。
      结果与SKBR-3相比，miR-5585-5p在耐药细胞SKBR-3/PR细胞株和外泌体中表达均上调（P < 0.01和P < 0.05）；在耐药细胞株中转染miR-5585-5p的抑制剂，Transwell、流式分析等结果显示，与对照相比，抑制剂组的耐药性下降，生物学活性降低（P < 0.01）；耐药细胞源性的外泌体与亲本细胞共培养可使SKBR-3细胞产生耐药表型，增强其迁移能力，抑制其凋亡率（P < 0.01），而转染抑制剂的耐药细胞分泌的外泌体可减弱这一作用。
      结论紫杉醇耐药乳腺癌细胞通过外泌体递送高表达的miR-5585-5p至亲本细胞并诱导亲本细胞产生耐药表型，外泌体miR-5585-5p可为乳腺癌耐药治疗提供新的分子靶点，为乳腺癌预后评估提供新的生物标志物。

       

      Abstract:
      ObjectiveTo study the effects of exosomal miR-5585-5p derived from paclitaxel-resistant breast cancer cells on the migration, apoptosis and drug resistance of breast cancer cells.
      MethodsThe exosomes were obtained by ultracentrifugation, and the expression levels of miR-5585-5p in breast cancer cell line(SKBR-3), paclitaxel-resistant breast cancer cell line(SKBR-3/PR) and exosomes were detected using qRT-PCR.The inhibitor of miR-5585-5p was transfected into paclitaxel-resistant breast cancer cells, the migration ability of cells was detected using Transwell assay, and the apoptosis of cells was detected using flow cytometry.The qRT-PCR and western blotting were used to detect the expression levels of drug-resistant gene.
      ResultsCompared with SKBR-3 cell line, the expression levels of miR-5585-5p in drug-resistant SKBR-3/PR cell line and exosomes were up-regulated(P < 0.01 and P < 0.05).After the miR-5585-5p inhibitor was transfected into the drug-resistant cell line, the results of Transwell assay and flow cytometry showed that the drug resistance and biological activity in the inhibitor group decreased compared with the control group(P < 0.01).The co-cultured drug-resistant cell-derived exosomes with breast cancer cells could induce the drug-resistant phenotype, enhance the ability of migration and inhibit the apoptosis rate of SKBR-3 cells(P < 0.01).However, the exosomes derived from drug-resistant breast cancer cells transfected with miR-5585-5p inhibitor could reduce the effects.
      ConclusionsThe paclitaxel-resistant breast cancer cells can deliver the highly expressed miR-5585-5p to the parent cells through exosomes, and induce the parent cells to produce drug-resistant phenotypes.The exosome miR-5585-5p can provide new molecular targets for the treatment of breast cancer drug-resistance, and provide new biomarkers for the prognosis assessment of breast cancer.

       

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