ZCCHC14调控的Akt/GSK3β/β-catenin信号转导是加速肝细胞癌增殖的罪魁祸首。

Q2 Medicine Journal of Buon Pub Date : 2021-09-01

Yujun Cui, Jijun Zhang, Chiyi Chen, Jinxuan Luo, Hao Yan, Wentao Jiang

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引用次数: 0

摘要

目的：阐明 ZCCHC14 如何影响肝细胞癌（HCC）的发展：方法：研究了ZCCHC14在HCC组织和细胞中的不同水平。采用 5-乙炔基-2'-脱氧尿苷（EdU）和 Transwell 试验分别检测过表达或敲除 ZCCHC14 的 HCC 细胞的增殖和迁移变化。测定了ZCCHC14介导的p-Akt/Akt、p-GSK3β/GSK3β和β-catenin在HCC细胞中的表达变化。在p-Akt激活剂SC79或β-catenin过表达的干预下，进一步验证了ZCCHC14介导的Akt/GSK3β/β-catenin信号转导参与了HCC细胞表型：结果：ZCCHC14在HCC中的上调加速了HCC细胞的体外增殖潜能。敲除 ZCCHC14 可使 Akt/GSK3β/β-catenin 信号失活，抑制 HCC 的恶性表型，而 SC79 诱导或过表达 β-catenin 可部分逆转这些表型：结论：通过激活Akt/GSK3β/β-catenin信号，ZCCHC14可加速HCC细胞增殖。

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The Akt/GSK3β/β-catenin signaling regulated by ZCCHC14 is responsible for accelerating the proliferation of hepatocellular carcinoma.

Purpose: To clarify how ZCCHC14 affects the development of hepatocellular carcinoma (HCC).

Methods: Differential levels of ZCCHC14 in HCC tissues and cells were examined. Proliferative and migratory changes in HCC cells with overexpression or knockdown of ZCCHC14 were detected using 5-Ethynyl-2'- deoxyuridine (EdU) and Transwell assay, respectively. Expression changes of p-Akt/Akt, p-GSK3β/GSK3β and β-catenin in HCC cells mediated by ZCCHC14 were determined. Intervened by the p-Akt activator SC79 or overexpression of β-catenin, further validated the involvement of the Akt/GSK3β/β-catenin signaling in HCC cell phenotypes mediated by ZCCHC14.

Results: Upregulated ZCCHC14 in HCC accelerated in vitro proliferative potential of HCC cells. Knockdown of ZCCHC14 inactivated the Akt/GSK3β/β-catenin signaling and inhibited malignant phenotypes of HCC, which were partially reversed by SC79 induction or overexpression of β-catenin.

Conclusions: By activating the Akt/GSK3β/β-catenin signaling, ZCCHC14 accelerates HCC cells proliferation.

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来源期刊

Journal of Buon 医学-肿瘤学

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.