Fig.1 PBK expression in 33 cancer types. A: Distribution of PBK mRNA expression in 33 cancer types and their normal controls based on TCGA data. B: Protein expression levels of PBK in different cancers based on data from the CPTAC database. C: ROC curve analysis of PBK in 33 cancer types, demonstrating its diagnostic ability to differentiate cancer from normal tissues. ***P<0.001, ****P<0.0001.

Fig.2 PBK expression in pancreatic cancer. A, B: TCGA and CPTAC data show significantly higher expression of PBK in pancreatic cancer tissues than in normal tissues. C-E: Differential expressions of PBK in pancreatic cancer and paired normal samples based on GSE16515, GSE15471 and GSE62165 datasets. F: Clinical feature heat map showing the association of PBK expression with pancreatic ductal adenocarcinoma and its correlation with tumor characteristics. G: ROC curves of the TCGA and GEO datasets further verify the reliability of PBK as a biomarker for diagnosis of pancreatic cancer. ***P<0.001, ****P<0.0001.

Fig.3 PBK is highly expressed in clinical samples and cell lines of pancreatic cancer. A: PBK protein expression levels in 4 clinical pancreatic cancer samples and their paired normal tissues. *P<0.05 vs Normal. B: PBK protein expression levels in normal pancreatic cell line HPDE6-C7 and 4 pancreatic cancer cell lines (PANC-1, AsPC-1, BxPC-3, and SW1990). *P<0.05 vs HPDE6-C7. C: PBK mRNA expression levels in 4 clinical pancreatic cancer samples and their paired normal tissues. ****P<0.0001. D: PBK mRNA expression levels in the normal pancreatic cell line HPDE6-C7 and 4 pancreatic cancer cell lines. *P<0.05 vs HPDE6-C7.

Fig.4 Prognostic value of PBK expression across 33 cancer types. A: Forest plot analysis of overall survival (OS) showing the prognostic value of PBK across various cancers. B: Forest plot analysis of disease-free survival (DFS) highlighting the potential impact of PBK in pancreatic cancer. C: Analysis of disease-specific survival (DSS) showing the ability of PBK for predicting disease-specific mortality. D: Progression-free survival (PFS) analysis further supports the role of PBK as a prognostic indicator.

Fig.5 PBK expression and its association with prognosis in pancreatic cancer. A: Kaplan-Meier survival curves show a significant association between high PBK expression and decreased OS. B: DFS survival curve validates the influence of PBK on disease-free survival. C: DSS survival curve highlights the relationship between high PBK expression and lower disease-specific survival. D: PFS survival curve reveals the connection between PBK expression and progression-free survival.

Fig.6 Univariate and multivariate analysis of the association of high PBK expression with prognosis of pancreatic cancer. A: Univariate analysis reveals significant association of PBK with clinicopathological factors of pancreatic cancer. B: Multivariate analysis validates PBK as an independent prognostic factor after adjusting for other clinical variables. C: A nomogram model for predicting survival probabilities of pancreatic cancer patients based on PBK expression. D: Calibration plot confirms the prediction accuracy of the nomogram model. E: ROC curves for 1-, 3-, and 5-year survival showing the predictive performance of PBK. *P<0.05, **P<0.01.

Fig.7 Gene correlation and enrichment analysis. A: Correlation analysis of PBK with 11 co-expressed genes across 33 cancer types. B: Intersection of PBK-related genes in pancreatic cancer, revealing key associated genes. C: GO analysis showing that PBK co-expressed genes are enriched in immune and cell cycle-related biological processes. D: KEGG pathway analysis shows that PBK is involved in cancer-related signaling pathways. E: GSEA analysis validates PBK-associated gene enrichment in immune regulation and tumor-related pathways.

Fig.8 PBK expression and tumor microenvironment analysis. A: Stromal Score analysis shows a correlation between PBK expression and tumor stromal content. B: Immune Score analysis indicates that PBK expression is associated with tumor immune infiltration. C: ESTIMATE Score analysis validates the role of PBK in the tumor microenvironment. D: Correlation between PBK expression and tumor mutation burden (TMB). E: Correlation between PBK expression and microsatellite instability (MSI), suggesting its potential immune regulatory mechanisms. *P<0.05, **P<0.01, ***P<0.001.

Fig.9 Relationship between PBK expression and immune system. A: Analysis of PBK expression and immune infiltration across 33 cancer types. B: Immune infiltration analysis of PBK in the pancreatic cancer immune microenvironment based on combined TCGA and GEO data. C: Correlation analysis of PBK expression with immune checkpoint molecules in 33 cancer types. D-F: Complex associations of PBK expression with MHC molecules (D), chemokines (E), and their receptors (F), suggesting its involvement in immune regulatory networks. *P<0.05, **P<0.01, ***P<0.001.

Fig.10 PBK expression and drug sensitivity analysis. A: Analysis from the CTRPC database shows that PBK mRNA expression affects drug sensitivity. B: Analysis from the GDSC database shows that PBK mRNA expression affects drug sensitivity. C: High PBK expression predicts poor response to gemcitabine treatment. D: High PBK expression is associated with chemotherapeutic drug resistance, indicating its potential as a drug target.

Fig.11 PBK knockdown inhibits proliferation, migration and invasion of pancreatic cancer cells. A: Western blotting showing efficient knockdown of PBK expression. B: Co-immunoprecipitation experiment shows that PBK directly interacts with NCAPG2, suggesting that the PBK-NCAPG2 axis plays a role in tumor progression. C: CCK-8 assay shows that PBK knockdown significantly inhibits cell proliferation. D: Transwell assay validating suppressed invasion ability of pancreatic cancer cells after PBK knockdown (Original magnification: ×200). E: Effect of shPBK on clone formation ability of pancreatic cancer cells. *P<0.05 vs shMock.