ArticleFunctional & integrative genomics2024
DKC1 aggravates gastric cancer cell migration and invasion through up-regulating the expression of TNFAIP6.
Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Loop of N2-polarized neutrophils and exhausted CD8 + T cells induces immunotherapy resistance in NSCLC.Molecular and cellular biochemistry · 2026Article
- Article
- Targeting DKC1/NF-κB axis suppresses tumorigenesis and enhances 5-FU sensitivity in gastric cancer.Cancer cell international · 2025Article
- METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation.Cellular and molecular life sciences : CMLS · 2025Article
- Revealing Potential Therapeutic Targets in Gastric Cancer through Inflammation and Protein-Protein Interaction Hub Networks.Journal of Cancer · 2025Article
- Pseudouridylation-Related Genes Predict Prognosis and Therapeutic Response in Hepatocellular Carcinoma Patients.Journal of Cancer · 2025Article
- Mutual antagonism between CD44 and integrins in glioblastoma cell traction and migration.APL bioengineering · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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