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首页> 外文期刊>Journal of cellular physiology. >NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition
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NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

机译：NFκB作为管理者应承担的癌症转移治疗反应:关注epithelial-mesenchymal过渡

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Abstract Metastasis of tumor cells is a complex challenge and significantly diminishes the overall survival and prognosis of cancer patients. The epithelial‐to‐mesenchymal transition (EMT) is a well‐known mechanism responsible for the invasiveness of tumor cells. A number of molecular pathways can regulate the?EMT mechanism in cancer cells and nuclear factor‐kappaB (NF‐κB) is one of them. The nuclear translocation of NF‐κB p65 can induce the transcription of several genes involved in EMT induction. The present review describes NF‐κB and EMT interaction in cancer cells and their association in cancer progression. Due to the oncogenic role NF‐κB signaling, its activation enhances metastasis of tumor cells via EMT induction. This has been confirmed in various cancers including brain, breast, lung and gastric cancers, among others. The ZEB1/2, transforming growth factor‐β, and Slug as inducers of EMT undergo upregulation by NF‐κB to promote metastasis of tumor cells. After EMT induction driven by NF‐κB, a significant decrease occurs in E‐cadherin levels, while N‐cadherin and vimentin levels undergo an increase. The noncoding RNAs can potentially also function as upstream mediators and modulate NF‐κB/EMT axis in cancers. Moreover, NF‐κB/EMT axis is involved in mediating drug resistance in tumor cells. Thus, suppressing NF‐κB/EMT axis can also promote the sensitivity of cancer cells to chemotherapeutic agents.
机译：抽象的肿瘤细胞的转移是一个复杂的挑战和显著减少癌症的整体生存和预后病人。过渡(EMT)是一个好机制负责肿瘤细胞的侵袭性。大量的分子途径可以调节的吗?地理因素所致kappaB (NFκB)就是其中之一。易位的NFκB p65可以诱导参与EMT的几个基因的转录归纳。EMT在癌细胞和他们互动协会在癌症的发展过程中。NFκB信号应承担的致癌作用,其激活通过EMT增强肿瘤细胞的转移归纳。癌症包括大脑、乳腺癌、肺癌和胃癌癌症等等。生长因子高β和蛞蝓EMT的诱导物接受upregulation, NFκB促进转移的肿瘤细胞。NFκB应承担的推动下,出现显著下降E钙粘素应承担的水平,而N的钙粘蛋白和波形蛋白水平进行增加。也可以作为上游吗中介和调节NFκB / EMT轴癌症。此外,NFκB / EMT应承担的轴是参与调解肿瘤细胞的耐药性。NFκB / EMT应承担的轴也可以促进敏感性肿瘤细胞化疗药物。

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  • 来源
    《Journal of cellular physiology.》 |2022年第7期|2770-2795|共26页
  • 作者

    Sepideh Mirzaei; Sam Saghari; Farzaneh BassiriRasoul RaesiAli ZarrabiKiavash HushmandiGautam SethiVinay Tergaonkar;

  • 作者单位

    Department of Biology, Faculty of Science, Science and Research Branch,Islamic Azad University;

    Department of Health Services Management, Tehran Medical Sciences,Islamic Azad University;

    Department of Biology, Fars Science and Research Branch,Islamic Azad UniversityPhD in Health Services Management,Mashhad University of Medical SciencesDepartment of Biomedical Engineering, Faculty of Engineering and Natural Sciences?,IstinyeDepartment of Pharmacology, Yong Loo Lin School of Medicine,National University of SingaporeLaboratory of NF‐κB Signaling,Institute of Molecular and Cell Biology (IMCB), 61 Biopolis DriveDepartment of Food Hygiene and Quality Control, Division of Epidemiology and Zoonoses, Faculty of;

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