Previous studies have indicated that centromere protein K (CENPK) is upregulated in several cancers and related to tumorigenesis. Nevertheless, the potential function of CENPK in gastric cancer (GC) remains unknown. Here, we investigated the function of CENPK on oncogenicity and explored its underlying mechanisms in GC. Our results showed that CENPK was dramatically overexpressed in GC and was associated with poor prognosis through bioinformatics analysis. We demonstrated that CENPK is upregulated in GC tissues and cell lines. Moreover, knockdown of CENPK significantly inhibited proliferation in vitro and attenuated the growth of implanted GCs in vivo. In addition, CENPK silencing induced G1 phase cell cycle arrest and facilitated apoptosis of GC cells. KEGG pathway analysis indicated that the PI3K-AKT signalling pathway was considerably enriched. Knockdown of CENPK decreased the expression of PI3K, p-Akt (Ser437) and p-GSK3β (Ser9) in GC cells, and increased the expression of PTEN. In conclusion, this study indicated that CENPK was overexpressed in GC and may promote gastric carcinogenesis through the PTEN-PI3K-AKT signalling pathway. Thus, CENPK may be a potential target for cancer therapeutics in GC.

中文翻译：

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胃癌中 CENPK 的敲低通过 PTEN-PI3K-AKT 信号通路抑制细胞生长并促进细胞凋亡


先前的研究表明，着丝粒蛋白 K (CENPK) 在多种癌症中表达上调，并与肿瘤发生相关。然而，CENPK 在胃癌 (GC) 中的潜在功能仍不清楚。在这里，我们研究了 CENPK 对致癌性的作用，并探讨了其在 GC 中的潜在机制。我们的结果表明，CENPK 在 GC 中显着过度表达，并且通过生物信息学分析与不良预后相关。我们证明 CENPK 在 GC 组织和细胞系中上调。此外，CENPK 的敲低可显着抑制体外增殖并减弱体内植入的 GC 的生长。此外，CENPK沉默诱导G1期细胞周期停滞并促进GC细胞凋亡。 KEGG通路分析表明PI3K-AKT信号通路显着富集。敲低 CENPK 会降低 GC 细胞中 PI3K、p-Akt (Ser437) 和 p-GSK3β (Ser9) 的表达，并增加 PTEN 的表达。总之，本研究表明CENPK在GC中过度表达，并可能通过PTEN-PI3K-AKT信号通路促进胃癌发生。因此，CENPK 可能是 GC 癌症治疗的潜在靶点。