CDH2 (Cadherin 2)

Our findings demonstrate KLRG1 as a critical negative regulator of antitumor immunity and support KLRG1-cadherin blockade as a promising strategy for improving immunotherapy outcomes.

Gene expression analysis revealed decreased N-cadherin/CDH2 (p < 0.05) and SOD2 (p < 0.01) gene expression in the presence of CC, suggesting antimetastatic and prooxidant effects. These results indicate that direct exposure to CC does not promote aggressive melanoma cell behavior in vitro.

In vivo, NPTX2 overexpression promoted tumor growth, increased Ki67 positivity, and enhanced H3K18la modification co-localizing with CAIX at the invasive front. This study demonstrates that NPTX2 drives ccRCC progression through coordinated regulation of cell cycle, EMT, and glycolysis-driven histone lactylation, positioning it as a potential prognostic biomarker and therapeutic target.

Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways. Given its potential role in metabolic regulation, full insights into the function of PDX1 in PCa could contribute to improved treatment and prevention strategies, particularly for men with PCa and comorbidities such as obesity and diabetes.

Additionally, low vimentin and enhanced E-cadherin expression lead to downregulation of core EMT regulators, including SNAIL1 and ZEB1. In conclusion, TQ showed potential chemomodulatory effects on TAM against TNBC by reducing the expression of EMT-associated markers.

Clinically, JOSD1 is markedly upregulated in glioma tissues and its high expression predicts poor patient survival. Our findings nominate the JOSD1-Twist1 axis as a druggable vulnerability for invasive glioblastoma and support future development of JOSD1-targeted therapies.

In this study, SEPT9 overexpression was shown to contribute to the oncogenic phenotype of bladder cancer and could serve as a potential early-stage biomarker. Moreover, SEPT9 may offer new avenues for developing more effective targeted therapeutic approaches for bladder cancer. Future studies addressing this aspect will be important for better defining the role of SEPT9 across diverse bladder cancer contexts.

The efficacy of bicalutamide in prostate cancer cells is significantly influenced by extracellular pH. The drug exerts stronger cytotoxic, antimigratory, and proapoptotic effects at physiological pH (7.4) compared with acidic conditions (6.8).

UCHL3 is significantly upregulated in TNBC and drives tumor progression by promoting cell proliferation and activating EMT-mediated migration and invasion. These findings identify UCHL3 as a potential therapeutic target for TNBC treatment.

WSME increased ROS levels, arrested the cell cycle in S and G2-M phases, decreased the expression of mesenchymal markers, namely, vimentin, N-cadherin and increased levels of the epithelial marker E-cadherin in treated MDA-MB-231 cells. These findings suggest that VISCB, WITHE, and WFA have the potential to emerge as potential antimetastatic agents against breast cancer in the future.

Gene expression profiling revealed significant upregulation of EMT (VIM, CDH2) and ECM (COL5A1) markers in both cell lines cultured on the PLA/PCL composite, with HT-29 showing elevated stemness (CD133) and adhesion (ICAM1), while HCT116 exhibited a hybrid EMT phenotype. Collectively, this work highlights the potential of PLA/PCL electrospun scaffolds to bridge conventional 2D cultures and complex 3D systems, thereby advancing in vitro colorectal cancer modeling and therapeutic testing for preclinical evaluations.

The as-developed BCRG exhibits active tumor targeting, good biocompatibility, and pH-responsive drug release, thereby triggering PDT-induced immunogenic cell death to kill primary tumors, inhibiting Gli1 gene to block angiogenesis and EMT, alleviating tumor hypoxia, restricting distant metastasis, and activating anti-tumor immunity to prevent recurrence without any systemic toxicity. This work demonstrates a rational design strategy to develop a multifunctional nanoplatform for synergistic therapy against metastatic tumors.