What question did this study set out to answer?

This research aims to explore the role of PTK6 in pancreatic adenocarcinoma regarding diagnosis and prognosis, and its relation to immune cells.

May 1, 2026

Role of PTK6 in the diagnosis, prognosis, and immune infiltration of pancreatic cancer based on evidence from bioinformatics analysis and experimental validation.

Key Points

This research aims to explore the role of PTK6 in pancreatic adenocarcinoma regarding diagnosis and prognosis, and its relation to immune cells.
Expression profiles and clinical data extracted from TCGA and GEO databases.
Statistical analyses including Wilcoxon rank-sum test, Cox regression, and Kaplan-Meier plots.
In vitro cell experiments using CCK-8, RT‒qPCR, and western blot to verify findings on PTK6’s biological effects.
PTK6 shows high expression in pancreatic adenocarcinoma with AUC values of 0.935 (TCGA) and 0.796 (GEO).
High PTK6 expression correlates with shorter overall survival (HR = 2.08, 95% CI: 1.36-3.19, p < 0.001).
In vitro downregulation of PTK6 through siRNA resulted in reduced cell proliferation and altered autophagy markers.

Abstract

BACKGROUND: Pancreatic adenocarcinoma (PAAD) is a highly lethal malignancy characterized by a dismal prognosis and limited treatment options. Protein tyrosine kinase 6 (PTK6) is abnormally activated in multiple cancer types. Understanding the function of PTK6 in pancreatic cancer could reveal novel therapeutic targets and prognostic markers. METHODS: We extracted the expression profiles and clinical data of patients with pancreatic adenocarcinoma from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The Wilcoxon rank-sum test was used to compare PTK6 gene expression levels between tumor tissues and normal pancreatic tissues. Functional enrichment analysis, Cox regression analysis, and Kaplan-Meier plot analysis were employed to determine the prognostic value of PTK6. Single-sample gene set enrichment analysis (ssGSEA) and TIMER3.0 were used to evaluate immune cell infiltration. Finally, CCK-8, RT‒qPCR, colony formation, and western blot assays were performed in vitro cellular experiments to verify the biological effects of PTK6 on the malignant behaviour of pancreatic cancer. RESULTS: PTK6 is highly expressed in pancreatic adenocarcinoma, with its upregulation validated in both TCGA (AUC = 0.935) and GEO (AUC = 0.796) cohorts. Elevated PTK6 expression was correlated with shorter overall survival (HR = 2.08, 95% CI: 1.36-3.19, p < 0.001), and multivariate analysis revealed that N1 stage was an independent prognostic factor for OS. In addition, PTK6 expression was negatively correlated with immune cell infiltration and key immune checkpoint genes, with the strongest correlation observed for TIGIT (ρ = -0.316, p < 0.001). In vitro experiments revealed that downregulating PTK6 expression via siRNA inhibited cell proliferation and colony formation, concomitant with increased LC3-II/LC3-I ratio, suggesting a potential role in autophagy regulation. CONCLUSION: PTK6 could serve as a potential diagnostic and prognostic biomarker for PAAD and may participate in immune modulation and autophagy regulation. These findings, supported by multi-cohort bioinformatic analysis and preliminary experimental validation, highlight its prospective clinical value in prognosis evaluation, immunotherapy, and targeted therapy for PAAD.

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