白细胞介素-25作为胰腺癌免疫基因治疗的候选基因

Zahra Piri , Abdolreza Esmaeilzadeh , Mehri Hajikhanmirzaei
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引用次数: 25

摘要

胰腺癌是一种侵袭性恶性肿瘤。一般来说,它的促进和进展是由于一些细胞和分子机制的干扰,特别是程序性细胞死亡或凋亡的失调。当然,在细胞生成和死亡之间失去平衡将导致各种组织的肿瘤团块发展,如胰腺。从几十年前开始,为了治疗胰腺癌,已经采用了化疗、放疗和手术等各种治疗方法,这些治疗方法与医疗结果不佳有关。因此,关于细胞因子白介素-25 (IL-25)的抗癌和促凋亡特性,作者打算预测一种新的治疗策略。IL-25,又称IL-17E,是死亡受体介导途径的主要因子之一。广泛地说,它的受体位于多种细胞上,如胰腺癌细胞。我们建议选择四组C57BL/6小鼠,以间充质干细胞为载体接种IL-25基因,以增加癌细胞对IL-25的暴露。IL-25可激活肿瘤坏死因子受体相关因子(TRAF6)、死亡结构域fas相关蛋白(FADD)和半胱天冬酶等凋亡介质。该方法可能通过诱导胰腺肿瘤细胞凋亡,在胰腺恶性肿瘤的治疗中发挥重要作用。
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Interleukin-25 as a candidate gene in immunogene therapy of pancreatic cancer

Pancreatic cancer is an aggressive type of malignancy. Generally, its promotion and progression are due to the disturbance in some cellular and molecular mechanisms, particularly deregulation of programmed cell death or apoptosis. Certainly, loss of counterbalance between generation and cell death will lead to the tumoural mass development in various tissues, such as pancreas.

From earlier decades, a variety of treatments as chemotherapy, radiation and surgery have been employed in order to pancreatic cancer remedial purposes, which are associated with infirm medical outcome. Therefore, with regard to the anti-cancerous and pro-apoptotic properties of the cytokine interleukin-25 (IL-25), the authors intend to anticipate a new therapeutic strategy. IL-25 – known as IL-17E – is one of the major factors responsible for death receptor-mediated pathway. Broadly, its receptor is located on multifarious cells such as pancreatic cancerous cells. We proposed to select four groups of C57BL/6 mice, for IL-25 gene inoculation, via mesenchymal stem cells as a vector, in order to increase exposure of cancerous cells to IL-25. IL-25 could activate apoptotic mediators including tumour necrosis factor receptor associated factor (TRAF6), Fas-Associated protein with Death Domain (FADD) and caspases consequently. Probably this method will be efficient in pancreatic malignancy treatment, via inducing apoptosis in pancreatic tumoural cells.

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Contents Editorial Board Editorial Board Contents Reprogramming of adult stem/progenitor cells into iPSCs without reprogramming factors
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