PBK (PDZ Binding Kinase)

High PBK expression was associated with longer OS and RFS and remained an independent favorable prognostic factor in multivariate analysis. PBK expression in CRC is linked to proliferative tumor epithelial states, an immune-activated microenvironment, and favorable outcomes, supporting its utility as a prognostic biomarker.

[This retracts the article DOI: 10.3892/etm.2018.6020.].

Given its central role in cancer progression, TOPK represents a promising candidate for novel cancer therapies. Additionally, we explore the therapeutic potential of targeting TOPK in cancer treatment, highlighting ongoing research efforts and the challenges in translating TOPK inhibition into clinical practice.

Third, they dispute the unrealistic survival curve in Fig. 2, suggesting evidence-based adjustments to reflect clinical plausibility. The letter emphasizes that addressing these concerns would strengthen the findings' impact on HCC research.

PBK is a key regulator of pancreatic cancer and interacts with NCAPG2 to promote tumor progression, suggesting its value as a potential biomarker and therapeutic target for pancreatic cancer.

Methionine deprivation through MEGL-targeted gene therapy may be a viable option for inducing cancer cell death compared to unrestricted levels of methionine.

PBK synergistically drives HCC progression through three synergistic mechanisms: (1) promoting oncogenic mutation accumulation (eg, TP53), (2) increasing metastatic potential, and (3) reprogramming an immune-suppressive microenvironment enriched for SPP1(+) macrophages and CD8(+)SLC4A10(+) MAIT cells. This establishes PBK as a dual-purpose biomarker for prognostic stratification and immunotherapy resistance prediction, providing a mechanistic rationale for developing PBK-targeted therapies in HCC.

Additionally, our study revealed that PBK genetic deletion alleviated the course of LPS-mediated neuroinflammation in vitro and in vivo, and AB did not exhibit any extra effects in LPS-mediated PBK-/- mice. These findings first offered broader prospects for treating neuroinflammation by targeting PBK to repress inflammation and activate autophagy, suggesting that AB had the potential to serve as a direct inhibitor in the PBK-TIPE2 interaction.

These findings establish TOPK as a central regulator of solar UV-induced skin carcinogenesis, partially via modulation of IL19 signaling and fibroblast activation. Targeting TOPK may offer a novel strategy for the prevention and treatment of NMSC.

Multivariable Cox regression analysis, incorporating stage and OXTR mRNA expression, demonstrated that PBK mRNA expression was the strongest independent predictor of OS. Our findings indicate that PBK plays a crucial role in the aggressiveness of mesothelioma, making it a promising therapeutic target and potential prognostic biomarker for mesothelioma.

PBK/TOPK is overexpressed in breast cancer tissues, and high expression levels are associated with poor patient prognosis. Additionally, PBK/TOPK is linked to immune infiltration in breast cancer, positively correlating with CD4+ and CD8+ T cells infiltration, suggesting a new avenue for immunotherapy research in breast cancer.

A group of genes, such as EIF4E, were closely associated with PBK expression and functions. These findings may provide insight into the molecular mechanism of PBK in GBM.