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首页> 外文期刊>Anti-cancer drugs >The role of the globular heads of the C1q receptor in paclitaxel-induced human ovarian cancer cells apoptosis by a mitochondria-dependent pathway
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The role of the globular heads of the C1q receptor in paclitaxel-induced human ovarian cancer cells apoptosis by a mitochondria-dependent pathway

机译：C1Q受体在紫杉醇诱导的人卵巢癌细胞凋亡的作用受到线粒体依赖性途径的凋亡

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摘要

As a mitochondrial membrane protein, globular C1q receptor (gC1qR) can mediate a variety of biological responses. Our study aims to investigate the role of gC1qR in paclitaxel-induced apoptosis of human ovarian cancer cells and to elucidate its potential molecular mechanism. The level of gC1qR was examined using real-time PCR and western blot analyses. Human ovarian cancer cells viability, migration, and proliferation were detected using the water-soluble tetrazolium salt (WST-1) assay, the transwell assay, and H-3-thymidine incorporation into DNA (H-3-TdR) assay, respectively. Apoptosis in cells was assessed using flow cytometric analysis. The intracellular reactive oxygen species was estimated by the fluorescence of H(2)DCFDA and the mitochondrial membrane potential was tested using a JC-1 probe. The expression of the gC1qR gene decreased significantly in human ovarian cancer tissues relative to the surrounding non-neoplastic ovarian tissues. Cells treated with paclitaxel showed increased gC1qR gene expression, cell apoptosis, and mitochondria dysfunction, and the effects on these cells could be abrogated by the addition of gC1qR small-interfering RNA or -lipoic acid that was used to protect the mitochondria function. In summary, these data support a mechanism that gC1qR-induced mitochondria dysfunction was involved in the paclitaxel-mediated apoptosis of ovarian cancer cells.
机译：作为线粒体膜蛋白，球状C1Q受体（GC1QR）可以介导各种生物反应。我们的研究旨在探讨GC1QR在紫杉醇诱导人卵巢癌细胞凋亡中的作用，并阐明其潜在的分子机制。使用实时PCR和Western印迹分析检查GC1QR的水平。使用水溶性四唑鎓盐（WST-1）测定，Transwell测定和H-3-胸苷掺入DNA（H-3-TDR）测定中检测人卵巢癌细胞活力，迁移和增殖。使用流式细胞术分析评估细胞中的细胞凋亡。通过H（2）DCFDA的荧光估计细胞内反应性氧物质，使用JC-1探针测试线粒体膜电位。 GC1QR基因的表达在人卵巢癌组织中相对于周围的非肿瘤卵巢组织显着下降。用紫杉醇处理的细胞显示出GC1QR基因表达，细胞凋亡和线粒体功能障碍的增加，并且通过添加GC1QR小干扰RNA或-Lipice酸可以消除对这些细胞的影响，用于保护线粒体功能。总之，这些数据支持GC1QR诱导的线粒体功能障碍参与卵巢癌细胞的紫杉醇介导的凋亡。

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  • 来源
    《Anti-cancer drugs》 |2018年第2期|共11页
  • 作者

    Lv Kang-Tai; Gao Ling-Juan; Hua Xiangdong; Li Fengshan; Gu Yun; Wang Wei;

  • 作者单位

    Nanjing Med Univ Qixia Dist Matern &

    Child Hlth Care Hosp Dept Gynaecol &

    Obstet Nanjing;

    Nanjing Med Univ Obstet &

    Gynecol Hosp Nanjing Matern &

    Child Hlth Care Hosp Dept Pathol;

    Nanjing Med Univ Obstet &

    Gynecol Hosp Nanjing Matern &

    Child Hlth Care Hosp Dept Pathol;

    Nanjing Med Univ Obstet &

    Gynecol Hosp Nanjing Matern &

    Child Hlth Care Hosp Dept Pathol;

    Nanjing Med Univ Obstet &

    Gynecol Hosp Nanjing Matern &

    Child Hlth Care Hosp Dept Pathol;

    Nanjing Med Univ Obstet &

    Gynecol Hosp Nanjing Matern &

    Child Hlth Care Hosp Dept Pathol;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药品;
  • 关键词

    apoptosis; gC1qR gene; mitochondria function; ovarian cancer cells; paclitaxel;

    机译：细胞凋亡;GC1QR基因;线粒体功能;卵巢癌细胞;紫杉醇;

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