DDX46通过激活MAPK-p38信号通路加速胶质母细胞瘤的增殖。

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

Ji Ma, Zhenying Gao, Xueni Liu

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引用次数: 0

摘要

目的:分析DDX46对胶质母细胞瘤(GBM)增殖和迁移潜能的影响。方法:采用实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction, qRT-PCR)和Western blot检测GBM患者与对照组DDX46的差异水平。通过DDX46干预U87和U251细胞，分别用菌落形成法、5-乙基-2′-脱氧尿苷(EdU)法和Transwell法检测其增殖和迁移的变化。检测DDX46或p38 MAPK抑制剂干预的GBM细胞中p-p38、p38、cyclin D1和MMP7的蛋白水平。结果:DDX46在GBM中表达上调。低表达DDX46可降低GBM细胞的增殖能力，而过表达DDX46可提高细胞的增殖率。DDX46对GBM的迁移能力没有影响。过表达DDX46可上调GBM细胞中的p-p38和cyclin D1。DDX46对GBM增殖的调节作用可被多马莫德部分逆转。结论:DDX46在GBM中表达上调，通过激活MAPK-p38信号通路增强GBM的增殖能力。

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DDX46 accelerates the proliferation of glioblastoma by activating the MAPK-p38 signaling.

Purpose: To analyze the influence of DDX46 on the proliferative and migratory potentials of glioblastoma (GBM).

Methods: Differential levels of DDX46 in GBM cases and controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. By intervening DDX46 in U87 and U251 cells, proliferative and migratory changes were determined by colony formation assay, 5-Ethynyl-2'- deoxyuridine (EdU) assay and Transwell assay, respectively. Protein levels of p-p38, p38, cyclin D1 and MMP7 in GBM cells intervened by DDX46 or the inhibitor of p38 MAPK were detected.

Results: DDX46 was upregulated in GBM cases. Knockdown of DDX46 attenuated the proliferative capacity of GBM cells, and its overexpression enhanced the proliferative rate. The migratory capacity of GBM was not affected by DDX46. Overexpression of DDX46 upregulated p-p38 and cyclin D1 in GBM cells. The regulatory effect of DDX46 on GBM proliferation could be partially reversed by the treatment of doramapimod.

Conclusions: DDX46 is upregulated in GBM, which strengthens the proliferative capacity of GBM by activating the MAPK-p38 signaling.

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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.