NEK2 通过 FOXM1/c-Myc/p27 信号通路抑制细胞衰老,从而促进 ESCC 恶性进展。

IF 3 2区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular Carcinogenesis Pub Date : 2024-11-06 DOI:10.1002/mc.23839
Jiachen Li, Yaojie Wang, Sisi Wei, Shi Xu, Suli Dai, Li Zhang, Ziqiang Tian, Lianmei Zhao, Huilai Lv
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引用次数: 0

摘要

有丝分裂永不有丝分裂基因A(NIMA)相关激酶2(NEK2)是一种参与细胞有丝分裂过程的重要丝氨酸-苏氨酸激酶。然而,NEK2与食管鳞状细胞癌(ESCC)之间的确切关系仍未得到充分了解。通过生物信息学分析、逆转录-定量 PCR(RT-qPCR)和免疫组织化学方法评估了 NEK2 在 ESCC 组织中的表达,结果显示 NEK2 与 ESCC 患者的预后有关。研究人员利用培养的ESCC细胞和人正常食管上皮细胞(HEEC),通过体外和体内综合汇合算法、集落形成、伤口愈合、transwell和ESCC异种移植肿瘤模型,研究了敲除NEK2对ESCC发生和发展的影响。研究发现,在 ESCC 组织中,NEK2 明显上调,其表达与 ESCC 患者的不良预后相关。NEK2 可能通过调节细胞增殖、迁移和侵袭促进 ESCC 的发展。此外,体内实验结果表明,敲除 NEK2 可抑制肿瘤生长。此外,研究还发现叉头盒 M1(FOXM1)是 NEK2 调控 ESCC 的潜在下游靶点,其过表达可逆转 NEK2 敲除对 ESCC 的影响。机理研究还表明,NEK2可能通过激活FOXM1/c-Myc/p27信号通路抑制细胞衰老,从而促进ESCC的恶性进展,这为ESCC的治疗提供了新的视角。
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NEK2 Promotes ESCC Malignant Progression by Inhibiting Cellular Senescence via the FOXM1/c-Myc/p27 Signaling Pathway.

Never in mitosis gene A (NIMA)-related kinase 2 (NEK2) is a crucial serine-threonine kinase involved in the process of cell mitosis. However, the precise relationship between NEK2 and esophageal squamous cell carcinoma (ESCC) remains inadequately understood. NEK2 expression in ESCC tissues was assessed through bioinformatics analysis, reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry, revealing a correlation with ESCC patient prognosis. Cultured ESCC cells and human normal esophageal epithelial cells (HEEC) were used to investigate the effects of NEK2 knockdown on the development and progression of ESCC by integrated confluence algorithm, colony formation, wound-healing, transwell, and ESCC xenograft tumor model, in vitro and in vivo. In ESCC tissues, NEK2 was found to be significantly upregulated, and its expression correlated with poor prognosis in ESCC patients. NEK2 may facilitate ESCC development by regulating cell proliferation, migration, and invasion. Additionally, results from in vivo experiments suggested that NEK2 knockdown can inhibit tumor growth. Moreover, forkhead box M1 (FOXM1) was identified as a potential downstream target of NEK2 in the regulation of ESCC, with its overexpression reversing the effects of NEK2 knockdown on ESCC. Mechanistic studies also indicated that NEK2 may promote the malignant progression of ESCC by inhibiting cellular senescence through the activation of the FOXM1/c-Myc/p27 signaling pathways, which may provide a novel perspective for the management of ESCC.

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来源期刊
Molecular Carcinogenesis
Molecular Carcinogenesis 医学-生化与分子生物学
CiteScore
7.30
自引率
2.20%
发文量
112
审稿时长
2 months
期刊介绍: Molecular Carcinogenesis publishes articles describing discoveries in basic and clinical science of the mechanisms involved in chemical-, environmental-, physical (e.g., radiation, trauma)-, infection and inflammation-associated cancer development, basic mechanisms of cancer prevention and therapy, the function of oncogenes and tumors suppressors, and the role of biomarkers for cancer risk prediction, molecular diagnosis and prognosis.
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