6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 acts as a protein kinase to regulate glioblastoma progression by activating the AKT/forkhead box O1 pathway.
6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 acts as a protein kinase to regulate glioblastoma progression by activating the AKT/forkhead box O1 pathway.
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DOI：
10.18388/abp.2020_5789
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发表时间：
2022-02
影响因子：
1.7
通讯作者：
K. zhao;Chaojun Yu;Jin-guang Luo;Minhao Huang;Qian Wen;Ninghui Zhao
中科院分区：
文献类型：
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作者：
K. zhao;Chaojun Yu;Jin-guang Luo;Minhao Huang;Qian Wen;Ninghui Zhao
6-磷酸果糖-2-激酶/果糖-2,6-双磷酸酶4 （PFKFB4）的异常表达与肿瘤的发生发展密切相关，PFKFB4已被证明具有蛋白激酶的功能。然而，PFKFB4在胶质母细胞瘤（GBM）中起作用的分子机制尚不清楚。因此，在本研究中，我们评估了PFKFB4在GBM中的作用。与邻近组织相比，PFKFB4在GBM中高表达，其表达水平与总生存时间呈负相关。此外，PFKFB4的下调抑制了GBM细胞的增殖和侵袭，促进了细胞的凋亡。在异种移植肿瘤模型中，使用短发夹RNA敲除PFKFB4可抑制肿瘤生长。进一步研究表明，PFKFB4参与调控AKT信号通路。因此，PFKFB4作为一种蛋白激酶通过激活AKT/forkhead box O1通路来调节GBM的进展，这可能是GBM的潜在治疗靶点。
Abnormal expression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) is closely related to the occurrence and development of tumors, and PFKFB4 has been shown to function as a protein kinase. However, the molecular mechanisms through which PFKFB4 functions in glioblastoma (GBM) remain poorly understood. Accordingly, in this study, we assessed the roles of PFKFB4 in GBM. Compared to in adjacent tissues, PFKFB4 was highly expressed in GBM, and its expression level was negatively correlated with the overall survival time. In addition, knockdown of PFKFB4 inhibited the proliferation and invasion of GBM cells and promoted apoptosis. In a xenograft tumor model, tumor growth was inhibited by knockdown of PFKFB4 using short hairpin RNA. Further studies demonstrated that PFKFB4 is involved in regulating the AKT signaling pathway. Thus, PFKFB4 acts as a protein kinase to regulate GBM progression by activating the AKT/forkhead box O1 pathway, which may be a potential therapeutic target in GBM.