TK1 (Thymidine Kinase 1)

Moreover, the Wnt/β-catenin inhibitor XAV939 reduced lactate production and H3K18la levels. Here, we demonstrate that the glycolysis/H3K18la/TK1/β-catenin positive feedback loop exacerbates dysfunction in OSCC initiation. These findings reveal a novel link between epigenetic regulation and lactate-driven metabolic reprogramming, which may lead to the development of innovative lactylation treatment approaches for OSCC therapy.

CCNB2, GTSE1, TK1, and NUSAP1 are shared molecular drivers of LUAD and pneumonia, offering diagnostic, prognostic, and therapeutic potential. The online version contains supplementary material available at 10.1007/s10616-026-00940-w.

Our findings suggest that LMetSig can significantly improve LUAD patients' stratification alongside conventional pathological and clinical parameters. By distinguishing high-risk patients from those with more favorable prognosis, this approach has the potential for informing personalized treatment strategies and improving clinical decision-making.

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.