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Life sciences · Journal article
Journal of Cancer Research and Clinical Oncology · October 9, 2026
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Abstract Objective This study identifies TTK as a prognostic LUAD biomarker regulated by a ceRNA network, driving immune evasion and therapeutic resistance. Methods An integrated in silico approach was employed using OncoMX, KM Plotter, UALCAN, and GEPIA2 for expression and survival analysis. Protein expression and promoter methylation were examined via HPA and OncoDB. Immune infiltration was mapped using TIMER 2.0 and CellTracer. Finally, molecular docking evaluated the predicted docking score of clinical inhibitors and natural flavonoids against the TTK ATP-binding pocket. Results TTK showed marked overexpression across cancers, especially in lung cancer (log 2 FC = 4.10). Elevated TTK expression predicted poorer OS (HR = 1.62, P = 3.7e-15), notably in female smoker subgroups. Protein levels confirmed higher TTK in LUAD with strong mRNA–protein correlation ( R = 0.845). Promoter hypomethylation and hotspot mutations supported its deregulation. TTK expression correlated with reduced CD8⁺ ( R = − 0.208), CD4⁺ ( R = − 0.333), and haematopoietic stem cells ( R = − 0.658), but increased suppressive immune cells ( R = 0.65), indicating an immune-evasive microenvironment. Since BAY 1,217,389 and CFI-402,257 are established TTK inhibitors (docking score = − 9.128 and − 8.417 Kcal/mol, respectively), their docking scores compared with hesperidin (docking score = − 9.407 Kcal/mol) showed similar docking strength, suggesting potential as a natural TTK inhibitor and combination therapy candidate. Key regulatory molecules of TTK included TF E2F1, hsa-let-7b-5p (miRNA), and TMPO-AS1 (lncRNA), forming the ceRNA axis. qRT-PCR confirmed TMPO-AS1 and TTK upregulation and hsa-let-7b-5p downregulation in lung cancer cell lines. Conclusion TTK is associated with LUAD progression through a putative TMPO-AS1/hsa-let-7b-5p regulatory axis, promoting immune evasion and serving as a high-affinity target for hesperidin therapy.