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甲状腺癌自噬相关基因差异表达的临床意义及前瞻性分子机制综合分析

发布者:抗性基因网 时间:2021-09-17 浏览量:442

摘要

       甲状腺癌(TC)是最常见的内分泌恶性肿瘤,约占内分泌系统所有恶性肿瘤的 90%。尽管 TC 患者往往具有良好的预后,但其高发病率和淋巴结转移仍然是悬而未决的问题。自噬是维持细胞内稳态不可或缺的过程;然而,自噬在 TC 发生和发展的几个步骤中的作用尚未阐明。在这项研究中,我们首先确定了几个在 TC 发作时激发的自噬相关基因 (ARG)。随后,生物信息学分析暗示这些基因在几个增殖信号通路中受到明显干扰。此外,我们证明差异表达的 ARG 与几种侵袭性临床表现密切相关,包括晚期肿瘤分期和淋巴结转移。我们的研究进一步选择了预后 ARG,并基于三个关键基因(ATG9B、BID 和 B1DNAJB1)开发了预后特征,这些基因显示出预测 TC 预后的中等能力。总的来说,这项研究的结果表明 ARGs 破坏了增殖相关的途径,从而导致了侵袭性的临床表现。这些发现提供了对 ARG 作用的潜在分子机制及其临床意义的深入了解,并提供了具有潜在治疗意义的分类信息。

       Thyroid cancer (TC) is the most common endocrine malignancy, accounting for approximately 90% of all malignancies of the endocrine system. Despite the fact that patients with TC tend to have good prognoses, the high incidence rate and lymph node metastases remain unresolved issues. Autophagy is an indispensable process that maintains intracellular homeostasis; however, the role of autophagy in several steps of the initiation and progression of TC has not yet been elucidated. In this study, we first identified several autophagy-related genes (ARGs) that were provoked in the onset of TC. Subsequently, a bioinformatics analysis hinted that these genes were markedly disturbed in several proliferative signaling pathways. Moreover, we demonstrated that the differentially expressed ARGs were closely related to several aggressive clinical manifestations, including an advanced tumor stage and lymph node metastasis. Our study further selected prognostic ARGs and developed a prognostic signature based on three key genes (ATG9B, BID and B1DNAJB1), which displayed a moderate ability to predict the prognosis of TC. On the whole, the findings of this study demonstrate that ARGs disrupt proliferation-related pathways and consequently lead to aggressive clinical manifestations. These findings provide insight into the potential molecular mechanisms of action of ARGs and their clinical significance, and also provide classification information of potential therapeutic significance.

https://www.spandidos-publications.com/10.3892/ijo.2018.4404?text=fulltext