Gastric cancer (GC) is one hackneyed malignancy tumor accompanied by high death rate. DKC1 has been discovered to serve as a facilitator in several cancers. Additionally, it was discovered from one study that DKC1 displayed higher expression in GC tissues than in the normal tissues. Nevertheless, its role and regulatory mechanism in GC is yet to be illustrated. In this study, it was proved that DKC1 expression was upregulated in GC tissues through GEPIA and UALCAN databases. Moreover, we discovered that DKC1 exhibited higher expression in GC cells. Functional experiments testified that DKC1 accelerated cell proliferation, migration, and invasion in GC. Further investigation disclosed that the weakened cell proliferation, migration, and invasion stimulated by DKC1 knockdown can be reversed after TNFAIP6 overexpression. Lastly, through in vivo experiments, it was demonstrated that DKC1 strengthened tumor growth. In conclusion, our work uncovered that DKC1 aggravated GC cell migration and invasion through upregulating the expression of TNFAIP6. This discovery might highlight the function of DKC1 in GC treatment.

胃癌（GC）是一种常见的恶性肿瘤，死亡率很高。DKC1 已被发现在多种癌症中发挥促进作用。此外，一项研究发现，DKC1在GC组织中的表达量高于正常组织。然而，其在GC中的作用和调节机制仍有待阐明。本研究通过GEPIA和UALCAN数据库证明GC组织中DKC1表达上调。此外，我们发现DKC1在GC细胞中表现出较高的表达。功能实验证明DKC1加速GC中的细胞增殖、迁移和侵袭。进一步的研究表明，DKC1 敲低所刺激的细胞增殖、迁移和侵袭减弱可以在 TNFAIP6 过表达后逆转。最后，通过体内实验证明DKC1增强肿瘤生长。总之，我们的工作发现DKC1通过上调TNFAIP6的表达来加剧GC细胞的迁移和侵袭。这一发现可能会凸显 DKC1 在 GC 治疗中的功能。