TK1 (Thymidine Kinase 1)

Breast cancer patients presenting with high baseline TK1 expression are associated with significantly worse prognostic outcomes. Collectively, these findings support the clinical potential of TK1 assessment for prognostic risk stratification and treatment guidance, which merits further verification in large-scale, multicenter clinical trials.

Functional validation experiments targeting TK1, including RNA interference followed by proliferation (CCK-8, EdU), migration (Transwell), and wound healing assays, substantiated its role in promoting tumor aggressiveness. Collectively, our findings suggest that integrating metabolic gene signatures with immunological context offers a promising framework for precision oncology in lung adenocarcinoma.

Furthermore, compared to the siControl+Pi+CaCl2 group, the siTK1+Pi+CaCl2 group exhibited decreased expression of differentiation markers, increased expression of calcification markers, and a further reduced p-AKT/AKT ratio (all P<0.05). Integrated bioinformatics and cellular validation demonstrate a correlation between TK1 expression and vascular calcification, suggesting a potential protective role for TK1 in this pathological process.

TK1 knockdown in OSCC cell lines significantly impaired cell migration and wound-healing ability. Our findings suggest that TK1 plays an active role in promoting OSCC progression and may serve as a prognostic biomarker and potential therapeutic target for metastatic OSCC.

Radio-resistant meningioma cells exhibit enhanced DNA repair, migration, invasion, and altered cell cycle dynamics. TK1 was identified as a promising biomarker and therapeutic target for overcoming radio-resistance in meningiomas.

High-TK1 expression could be a potential indicator for therapeutic resistance, poor PFS and immune evasion in metastatic RCC under IO + TKI therapy. The novel RF risk score may help stratify patients for IO + TKI therapy.

Genes related with TK1 or TK2 were involved in pathways related to DNA replication, proteasome, and homologous recombination. Clinically, these findings suggest that the differential expression of TK1 and TK2 could serve as potential biomarkers, as well as therapeutic targets for personalized treatment strategies in CESC patients.

This dual role of TK1 drives the proliferation of human hepatocellular carcinoma cells and liver tumor growth in mice. Our findings reveal a crucial mechanism by which growth factors promote tumor development through TK1-mediated DNA synthesis and glycolysis and highlight TK1 as a potential molecular target for cancer treatment.

Analysis of immune infiltration revealed a negative correlation between TK1 and CD8 + T cells, macrophages, and dendritic cells. In vitro experiments, TK1 knockdown resulted in the inhibition of proliferation, migration, invasion and EMT in UCEC cell lines.

Creation of a protein-protein interaction map of TK1 and the pathogenic factors we evaluated predict that the majority of factors evaluated either directly or indirectly interact with TK1. Our findings argue that TK1 elevation directly increases HCC 1806 cell pathogenicity and is likely occurring by p21- and AKT3-mediated mechanisms to promote cell cycle arrest, cellular migration, and cellular survival.

When the regulatory network of LINC00665/has-let-7b-5p/TK1 was assessed, it was observed that elevated TK1 levels may affect the prognosis of NSCLC. Therefore, it could be considered a prognostic biomarker and a probable therapeutic target for predicting NSCLC prognosis.

We established a prognostic model related to Treg infiltration and this model can be used to establish a clinically relevant classification of TNBC progression. Additionally, our work revealed the underestimable potential of TK1 as a tumor biomarker and immunotherapeutic target.