CKAP4 (Cytoskeleton Associated Protein 4)

Notably, frequent phosphorylation of S146 across cancer types points to a potential tumor-specific regulatory role. Together, these findings provide the first systems-level insight into the role of MAST3 in cytoskeletal regulation and disease relevance.

The therapeutic potential of targeting CKAP4 is extensively explored, including novel approaches like anti-CKAP4 antibodies and aptamers, and their synergistic effects with existing treatments. By integrating findings from esophageal, gastric, pancreatic, and colorectal cancers, this review provides a unique, comprehensive overview of CKAP4 in GI oncology, underscoring CKAP4's potential to revolutionize GI cancer diagnosis and treatment and paving the way for future translational research.

The ferroptosis activator RSL3 further attenuated tumor progression in both the knockdown and overexpression models, and combined treatment with the ERK inhibitor SCH772984 synergistically suppressed tumor growth in MIR4435-2HG-overexpressing xenografts. Notably, RSL3 diminished IQGAP3, Ras, ERK, CREB, and GPX4 levels across the experimental conditions. These findings indicate that MIR4435-2HG is a pivotal regulator of bladder cancer progression and ferroptosis via the IQGAP3/Ras/ERK/CREB axis, suggesting that MIR4435-2HG is a potential therapeutic target for intervention.

Both genetic and pharmacological AEBP1 inhibition synergize with immune checkpoint blockade in syngeneic models. Our study establishes AEBP1 as a key regulator of CAF-mediated T cell dysfunction and a therapeutic target.

Moreover, CKAP4 has emerged as a key mediator linking extracellular matrix remodeling to inflammatory responses, which are closely associated with age-related diseases. This review comprehensively summarizes the current understanding of CKAP4's molecular mechanisms in cell longevity and aging, discusses its involvement in inflammation and tissue homeostasis, and explores its potential as a therapeutic target for aging-related disorders.

Moreover, blocking DKK1 promotes neutrophil maturation to improve the immune microenvironment, induces tumor shrinkage, and enhances ICB therapy response in multiple bone metastasis mouse models. These findings uncover a critical role for immature neutrophils in bone metastases and suggest a potential strategy for modulating neutrophils to improve cancer immunotherapy.

The biosensor may achieve a low detection limit of 0.30 pg/mL, with a broad linear range covering five orders of magnitude, and exhibits satisfying anti-interference ability in complex biological matrices. Furthermore, it displays outstanding discriminatory accuracy in differentiating ovarian cancer patient samples from healthy controls, showing great potential for cancer diagnosis.

In conclusion, this study identified CKAP4 and PLOD2 as novel prognostic protein markers for HCC. The developed nomogram, integrating these molecular markers with AJCC stage, shows promise in predicting OS and stratifying risk in HCC patients.

Notably, exercise training improved CRF-related gene expression and increased CD8+ T-cell infiltration, emphasizing the therapeutic potential of physical activity. These findings underscore the utility of CRF-related genes as prognostic markers in HCC and highlight the interplay between CRF and tumor immunity, offering novel insights for personalized treatment strategies.

Multivariate analysis showed that CKAP4-1 positivity was an independent predictor of RFS (p = 0.041, hazard ratio: 2.09, 95% confidence interval: 1.03-4.25). This study showed that CKAP4 expression in tumor cells may serve as a useful prognostic biomarker for patients with BCa who undergo RC.

High-risk patients responded better to AZD5991-1720, an MCL1 inhibitor, while low-risk patients showed improved responses to IGF1R-3801-1738, an IGF1R inhibitor, suggesting that risk stratification may help optimize treatment selection based on tumor-specific vulnerabilities...However, prospective validation is needed to confirm its clinical applicability. Potential limitations such as sample size and generalizability should be considered.

Targeting CKAP4 with masitinib or antibodies impairs P. micra attachment and abolishes P. micra-promoted OSCC metastasis in vitro and in vivo. Together, our findings identify P. micra as a pathogen that promotes OSCC metastasis and highlight that TmpC-CKAP4 interaction could be a potential therapeutic target for OSCC.