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首页> 外文期刊>Biotechnology and bioprocess engineering >Fisetin Inhibits Cell Proliferation and Induces Apoptosis via JAK/STAT3 Signaling Pathways in Human Thyroid TPC 1 Cancer Cells
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Fisetin Inhibits Cell Proliferation and Induces Apoptosis via JAK/STAT3 Signaling Pathways in Human Thyroid TPC 1 Cancer Cells

机译：Fisetin抑制细胞增殖并通过Jak / Stat3信号传导途径诱导人甲状腺TPC 1癌细胞中的凋亡

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摘要

Thyroid cancer is the most important malignant tumor reported in human populations where, its treatment remains undeveloped. Fisetin, a plant flavonoid exhibits several pharmacological properties like antioxidant, anti-inflammatory, and anticancer function. In the existing study, we assessed fisetin mediated cytotoxic effects and action potential of fisetin on cell proliferation in TPC-1 human cancer cells. Also, examined the apoptosis in TPC-1 cells by reactive oxygen species (ROS) generation, the mitochondrial membrane potential (MMP) and apoptotic morphological changes through AO/EtBr staining. Additionally, we analyzed the effects of fisetin through ELISA analysis to evaluate the caspases expression and studied JAK 1 and STAT3 signaling molecule in TPC1 cells. Our results demonstrated that fisetin stimulated apoptosis, which confirmed through reduced cell viability, improved ROS generation, altered MMP and cell cycle phases in TPC-1 cells. Further, the fisetin up-regulated the expression of caspase (3, 8, and 9) expressions in TPC-1 cells. Also, we observed the fisetin down-regulated the JAK 1 and STAT3 expression in TPC 1 cells. Thus, the fisetin induced apoptosis in TPC-1 cells by the induction of oxidative damage and enhanced caspases expression by down-regulating JAK 1 and STAT3 signaling molecules. Hence, the fisetin would be considered as a beneficial therapeutic agent for the thyroid cancer treatment.
机译：甲状腺癌是人口中报道的最重要的恶性肿瘤，其治疗仍未开发。 Fisetin，植物黄酮表现出几种药理学性质，如抗氧化剂，抗炎和抗癌功能。在现有的研究中，我们评估了在TPC-1人癌细胞中细胞增殖的Fisetin介导的细胞毒性效应和动作潜力。此外，通过AO / ETBR染色通过反应性氧物质（ROS）产生，线粒体膜电位（MMP）和凋亡形态变化来检查TPC-1细胞中的凋亡。另外，我们通过ELISA分析分析了Fisetin的影响，评价了TPC1细胞中的jak 1和stat3信号分子的jak 1和stat3信号分子。我们的研究结果表明，通过降低的细胞活力，改进的ROS产生，改善的ROS细胞，改善了TPC-1细胞中的Fisetin刺激凋亡。此外，Fisetin上调TPC-1细胞中的胱天蛋白酶（3,8和9）表达的表达。此外，我们观察到在TPC 1细胞中下调jak 1和stat3表达的Fisetin。因此，通过诱导氧化损伤和增强的胱天蛋白酶通过下调JAK 1和STAT3信号分子诱导氧化损伤和增强的胱天蛋白酶诱导凋亡。因此，Fisetin将被认为是甲状腺癌治疗的有益治疗剂。

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  • 来源
    《Biotechnology and bioprocess engineering》 |2020年第2期|197-205|共9页
  • 作者

    Ying Liang; Deyu Kong; Yi Zhang; Siqi Li; Yan Li; Anuradha Ramamoorthy; Junfeng Ma;

  • 作者单位

    Thyroid and Breast Surgery The Second Affiliated Hospital of Kunming Medical University Kunming Yunnan 650101 China;

    Internal Medicine-Oncology The First Affiliated Hospital of Kunming Medical University Kunming Yunnan 650032 China;

    Thyroid and Breast Surgery The Second Affiliated Hospital of Kunming Medical University Kunming Yunnan 650101 China;

    Thyroid and Breast Surgery The Second Affiliated Hospital of Kunming Medical University Kunming Yunnan 650101 China;

    Thyroid and Breast Surgery The Second Affiliated Hospital of Kunming Medical University Kunming Yunnan 650101 China;

    PG and Research Department of Biochemistry SengamalaThayaar Educational Trust Women's College Sundarakkottai Mannargudi Thiruvarur (Dt.) Tamil Nadu India;

    Thyroid and Breast Surgery The Second Affiliated Hospital of Kunming Medical University Kunming Yunnan 650101 China;

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  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    fisetin; thyroid cancer; apoptosis; JAK1/STAT3; caspase;

    机译：Fisetin;甲状腺癌;细胞凋亡;JAK1 / Stat3;Caspase.;

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