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CDCA8通过调控CDK1促进甲状腺癌的发生和发展。

CDCA8 Contributes to the Development and Progression of Thyroid Cancer through Regulating CDK1.

作者信息

Xiang Cheng, Sun Wu-Hui, Ke You, Yu Xing, Wang Yong

机构信息

Department of Thyroid Surgery, The Second Affiliated Hospital of Zhejiang University College of Medicine, Hangzhou, Zhejiang, China.

Department of Nephrology, The Second Affiliated Hospital of Zhejiang University College of Medicine, Hangzhou, Zhejiang, China.

出版信息

J Cancer. 2022 Apr 18;13(7):2322-2335. doi: 10.7150/jca.64747. eCollection 2022.

DOI:10.7150/jca.64747
PMID:35517403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9066215/
Abstract

: This study aims to reveal regulatory role of cell division cycle associated 8 (CDCA8) in thyroid cancer progression and metastasis. : A series of experiments and were performed to explore the function of CDCA8 in thyroid cancer. : Immunohistochemical analysis showed that CDCA8 expression levels were upregulated in thyroid cancer tissues compared with normal tissues, and were statistically correlated with tumor stage. Results of loss-of-function assay showed that downregulation of endogenous expression of CDCA8 could significantly inhibit cell proliferation, colony formation, cell migration, and promote apoptosis. Thyroid cancer cells lacking CDCA8 expression also had reduced tumorigenicity . Further, results of preliminary mechanistic exploration showed that CDK1 may be a potential downstream molecule of CDCA8 in regulating thyroid cancer progression. We subsequently confirmed that CDK1 itself exerted a significant regulatory function in thyroid cancer by loss- and gain-of-function experiments. Moreover, overexpression of CDK1 could weaken the tumor suppressive effect caused by CDCA8 knockdown. : CDCA8 functions as an oncogene in thyroid cancer, and CDCA8 knockdown suppresses cancer development and . Additionally, CDK1 was further identified as a potential target of CDCA8 in thyroid cancer.

摘要

本研究旨在揭示细胞分裂周期相关蛋白8（CDCA8）在甲状腺癌进展和转移中的调控作用。进行了一系列实验以探究CDCA8在甲状腺癌中的功能。免疫组织化学分析显示，与正常组织相比，甲状腺癌组织中CDCA8表达水平上调，且与肿瘤分期具有统计学相关性。功能丧失实验结果表明，内源性CDCA8表达下调可显著抑制细胞增殖、集落形成、细胞迁移，并促进细胞凋亡。缺乏CDCA8表达的甲状腺癌细胞的致瘤性也降低。此外，初步机制探索结果表明，CDK1可能是CDCA8在调节甲状腺癌进展中的潜在下游分子。随后，我们通过功能丧失和功能获得实验证实CDK1本身在甲状腺癌中发挥重要调控作用。此外，CDK1的过表达可减弱CDCA8敲低所引起的肿瘤抑制作用。CDCA8在甲状腺癌中作为癌基因发挥作用，CDCA8敲低可抑制癌症发展。此外，CDK1被进一步确定为甲状腺癌中CDCA8的潜在靶点。

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