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Trop2 promotes proliferation, invasion and EMT of nasopharyngeal carcinoma cells through the NF-kappa B pathway

机译:Trop2通过NF-Kappa B途径促进鼻咽癌细胞的增殖,侵袭和EMT

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摘要

Human trophoblast cell surface antigen 2 (Trop2), a cell surface transmembrane glycoprotein receptor, has been demonstrated to be closely associated with increasing tumor aggressiveness, metastasis and unfavorable prognosis. However, the biological roles of Trop2 and its underlying mechanism in nasopharyngeal carcinoma cells (NPC) are still unclear. In this study, we found that Trop2 was up-regulated in NPC tissues and cell lines compared with normal nasopharyngeal epithelial tissues and cells. Trop2 overexpression promoted cell proliferation, invasion and the EMT process and activated the NF-kappa B signaling pathway, while Trop2 downregulation showed the opposite effects in NPC cells. Moreover, NF-kappa B inhibitor pyrolidinedithiocarbamate (PDTC) or NF-kappa B knockdown attenuated Trop2-induced cell proliferation, invasion and EMT in NPC cells. Taken together, Trop2 accelerates cell proliferation, invasion and EMT in NPC via activating the NF-kappa B pathway, indicating that Trop2 may be exploited in targeted therapy for patients with NPC.
机译:人滋养细胞表面抗原2(TOF2),一种细胞表面跨膜糖蛋白受体,已经证明与增加肿瘤侵袭性,转移和不利预后密切相关。然而,Trop2及其潜在机制在鼻咽癌细胞(NPC)中的生物学作用尚不清楚。在本研究中,我们发现与正常的鼻咽上皮组织和细胞相比,Trop2在NPC组织和细胞系中调节。 Trop2过表达促进细胞增殖,侵袭和EMT过程并激活NF-Kappa发信号通路,而Trop2下调显示NPC细胞的相反效果。此外,NF-Kappa B抑制剂吡咯烷二氨基甲酸酯(PDTC)或NF-Kappa B敲低衰减的TOP2诱导的细胞增殖,侵袭和EMT。连胜,通过激活NF-Kappa途径加速细胞增殖,侵袭和EMT,表明Trop2可以在NPC患者中被利用。

著录项

  • 来源
    《RSC Advances》 |2017年第84期|共10页
  • 作者单位

    Henan Univ Huaihe Hosp Dept Otolaryngol Kaifeng 475000 Peoples R China;

    Henan Univ Huaihe Hosp Dept Otolaryngol Kaifeng 475000 Peoples R China;

    Henan Univ Huaihe Hosp Dept Oncol 8 Baobei Rd Kaifeng 475000 Peoples R China;

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

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