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首页> 外文期刊>Cancer Management and Research >CSNK2A1 Promotes Gastric Cancer Invasion Through the PI3K-Akt-mTOR Signaling Pathway
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CSNK2A1 Promotes Gastric Cancer Invasion Through the PI3K-Akt-mTOR Signaling Pathway

机译：CSNK2A1通过PI3K-AKT-MTOR信号通路促进胃癌入侵

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Objective: Casein kinase 2 a1 (CSNK2A1) has been shown to be involved in tumorigenesis by enhancing several oncogenic signaling pathways in various cancers. However, the function and mechanism of CSNK2A1 in gastric cancer remain unclear, and this study aimed to elucidate the role of CSNK2A1 in gastric cancer. Methods: CSNK2A1 expression was assessed by Western blot and qPCR in four gastric cancer (GC) cell lines and one normal gastric epithelial cell line. Stable cancer cell lines with CSNK2A1 gene overexpression or knockdown were established to investigate the function and mechanism of CSNK2A1 in GC cells. Results: CSNK2A1 expression was higher in GC cells than in normal gastric epithelial cells. Stable overexpression of CSNK2A1 in SNU216 cells significantly increased cellular proliferation, invasion, and migration. Silencing CSNK2A1 expression in SGC-790 cells effectively inhibited its oncogenic function. We further verified that epithelial-mesenchymal transition (EMT) was affected by CSNK2A1 and that CSNK2A1 promotes GC cell invasion through the PI3K-Akt-mTOR signaling pathway. Conclusion: Our findings suggested that CSNK2A1 plays important oncogenic roles in GC invasion via EMT and the PI3K-Akt-mTOR signaling pathway and that CSNK2A1 may serve as a novel prognostic and/or therapeutic target in GC.
机译：目的：通过在各种癌症中增强几种致癌信号通路，表明酪蛋白激酶2A1（CSNK2A1）已显示参与肿瘤发生。然而，CSNK2A1在胃癌中的功能和机制仍然尚不清楚，本研究旨在阐明CSNK2A1在胃癌中的作用。方法：在胃癌（GC）细胞系中的蛋白质印迹和QPCR评估CSNK2A1表达，以及一种正常胃上皮细胞系。建立稳定的癌细胞系具有CSNK2A1基因过表达或敲低的，以研究CSNK2A1在GC细胞中的功能和机制。结果：GC细胞中的CSNK2A1表达高于正常胃上皮细胞。 SNU216细胞中CSNK2A1的稳定过表达显着增加了细胞增殖，侵袭和迁移。 SGC-790细胞中的沉默CSNK2A1表达有效地抑制了其致癌功能。我们进一步验证了上皮 - 间充质转换（EMT）受CSNK2A1的影响，并且CSNK2A1通过PI3K-AKT-MTOR信号传导途径促进GC细胞侵袭。结论：我们的研究结果表明，CSNK2A1在GC侵袭通过EMT和PI3K-AKT-MTOR信号通路中起重要的致癌作用，并且CSNK2A1可以用作GC中的新型预后和/或治疗靶标。

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