PI3K/AKT/mTOR通路
胶质瘤
蛋白激酶B
小桶
基因敲除
癌症研究
生物
信号转导
细胞生长
细胞凋亡
细胞生物学
基因表达
基因
转录组
生物化学
作者
Yourui Zou,Ling Huang,Shibin Sun,Fangqian Yue,Zhuoqi Li,Yue Ma,Hui Ma
出处
期刊:Cancer Biotherapy and Radiopharmaceuticals
[Mary Ann Liebert]
日期:2021-11-16
被引量:7
标识
DOI:10.1089/cbr.2021.0294
摘要
Objective: The most commonly reported primary brain tumor in adults is glioma. Choline kinase alpha (CHKA) has been proved to play important roles in glioma. However, the mechanism of CHKA involved remains unclear. Therefore, this study aims to explore the mechanism of CHKA in glioma development. Methods: Immunohistochemistry, qRT-PCR, and Western blot were used to detect the expression of CHKA. Flow cytometry, Cell Counting Kit-8 (CCK-8), transwell, and wound healing assays were performed to evaluate cell apoptosis, proliferation, invasion, and migration, respectively. RNA sequencing was used to explore the differentially expressed genes affected by CHKA. The enrichment analysis of gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) helped to detect the signaling pathways CHKA affected. Tumor-bearing mice were established and evaluated by TUNEL assay, Ki-67 immunohistochemistry. and hematoxylin and eosin staining. Results:CHKA increased in glioma tissues and promoted cell proliferation, invasion, and migration, while inhibiting the glioma cell apoptosis. It was also showed that CHKA promoted glioma development in vivo. GO and KEGG analysis indicated that PI3K/AKT was significantly enriched in CHKA knockdown U251 cells. And CHKA promoted glioma development by activating PI3K/AKT signaling pathway. Conclusions: The authors demonstrated that CHKA was significantly elevated in glioma tissues. Mechanism analysis indicated that CHKA could promote glioma development by activating PI3K/AKT signaling pathway, suggesting that CHKA is promising to be a biomarker and therapeutic strategy for prognostic prediction of patients with glioma.
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