AURKA在胃癌中的致癌作用:机制、途径和临床相关性。

IF 2.9 3区 医学 Q2 ONCOLOGY
Caixia Lv, Yan Liu, Huanhu Zhang
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引用次数: 0

摘要

极光激酶A (AURKA)是一种丝氨酸/苏氨酸激酶,在细胞周期调节中起关键作用,特别是在有丝分裂过程中。最近的研究发现AURKA在包括胃癌(GC)在内的多种癌症中是一个过表达的癌基因。本文就AURKA参与胃癌发病的分子机制进行综述,包括其在细胞增殖、细胞凋亡抑制、上皮-间质转化(epithelial-mesenchymal transition, EMT)和癌变中的作用。AURKA调节PI3K/Akt、Wnt/β-catenin、NF-κB、JAK2/STAT3等关键信号通路,促进肿瘤生长、转移和耐药。此外,AURKA与p53和PTEN等关键肿瘤抑制因子相互作用,进一步增强其致癌潜力。临床研究表明,AURKA过表达与GC患者预后不良相关,凸显了其作为诊断和治疗靶点的潜力。这篇综述还讨论了AURKA抑制剂在临床前的疗效,提供了对其治疗潜力的见解。通过阐明AURKA在GC中的多方面作用,本文旨在全面了解其机制及其对未来研究和治疗策略的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Oncogenic Role of AURKA in Gastric Cancer: Mechanisms, Pathways, and Clinical Relevance.

Aurora kinase A (AURKA) is a serine/threonine kinase that plays a critical role in cell cycle regulation, particularly during mitosis. Recent studies have identified AURKA as an oncogene overexpressed in various cancers, including gastric cancer (GC). This review summarizes the molecular mechanisms by which AURKA contributes to GC pathogenesis, including its roles in cell proliferation, apoptosis inhibition, epithelial-mesenchymal transition (EMT), and cancer stemness. AURKA regulates key signaling pathways such as PI3K/Akt, Wnt/β-catenin, NF-κB, and JAK2/STAT3, promoting tumor growth, metastasis, and therapy resistance. Additionally, AURKA interacts with critical tumor suppressors like p53 and PTEN, further enhancing its oncogenic potential. Clinical studies have demonstrated that AURKA overexpression correlates with poor prognosis in GC patients, highlighting its potential as a diagnostic and therapeutic target. This review also discusses the efficacy of AURKA inhibitors in preclinical settings, offering insights into their therapeutic potential. By elucidating the multifaceted roles of AURKA in GC, this review aims to provide a comprehensive understanding of its mechanisms and implications for future research and treatment strategies.

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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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