ACKR3 (Atypical Chemokine Receptor 3)

A mechanistic approach revealed that RD-20 suppresses NF-κB activation, thereby blocking the expression of CXCR4, MMP-2, and MMP-9. Collectively, these findings indicate that RD-20 abrogates the NF-κB activation to induce anti-EMT effects in PC cells.

Biomarkers based on GPCR expression, Hippo activity, and immune cell spatial signatures are critical for patient stratification. Future research should leverage single-cell multi-omics, spatial biology, and machine learning to decipher cell-specific signaling within the TME and accelerate the translation of immune-modulating combinatorial therapies.

We also evaluate therapeutic opportunities, including CXCR4/CXCR7 antagonists, CXCL12-neutralizing strategies, and biomarker-guided combinations with targeted therapies or immunotherapies. We propose that this axis should be approached not as a uniformly pathogenic pathway, but as a context-dependent spatial system whose therapeutic modulation must be tailored to viral species, tissue compartment, disease stage, and receptor state.

We developed a CRISPR-Cas9 screening-based prognostic signature for BC that effectively stratifies patient risk and demonstrates robust predictive performance across cohorts. CHORDC1 was identified as a key oncogenic driver, promoting tumor progression via pathways such as EMT and mTORC1 signaling, highlighting its potential as a therapeutic target. These findings may contribute to the development of personalized prognostic tools and therapeutic strategies in BC.

Here, we describe an optimized protocol for the ibidi 3D µ-Slide chemotaxis assay to study MIF-mediated pro-migratory effects on human neutrophils, a prototype of innate immune cells, and CD4+ T cells, a cornerstone of adaptive immunity. Additionally, we discuss the application of current inhibitor strategies to selectively target and identify the receptor pathways involved.

Tumor CXCR7 expression is associated with reduced lymphocytic infiltration and an immune-excluded phenotype in HGSC, suggesting a potential role of the CXCR7 axis in shaping the tumor immune microenvironment.

Preclinical studies demonstrate that CXCR4 antagonists (e.g., plerixafor, LY2510924) suppress metastasis and, when combined with immune checkpoint inhibitors, can reverse the "cold" immune phenotype of microsatellite-stable CRC. We also discuss recent advances in the regulation of CXCL12/CXCR4 expression, the role of related receptors such as CXCR7, and emerging strategies targeting this axis for therapeutic intervention. Collectively, current evidence supports the CXCL12/CXCR4 axis as a promising biomarker and therapeutic target in metastatic CRC, and further elucidation of its regulatory network may facilitate the development of more effective precision treatment strategies.

This study reveals that NETs-associated genes play crucial roles in colon cancer progression, immune modulation, and metabolic reprogramming. The identified four-gene signature may serve as a candidate biomarker for risk stratification in colon cancer, although further validation is needed.

ELISA assays confirmed dose-dependent CXCR4 downregulation with negligible effects on CXCR7, indicating high functional selectivity. Overall, this integrative strategy accelerates the discovery of potent, selective CXCR4 inhibitors for translational research.

The study identified the primary oridonin targets during psoriasis treatment using network pharmacology. Bioinformatics analysis with empirical verification demonstrated strong associations between SIRT1, CDK2, SRC, PTPN1, TP53, HSP90AA1, and EGFR and oridonin. These interactions were positively correlated with an inhibition of proliferation and angiogenesis mediated by blocking PI3K-Akt signaling pathway.

Interestingly, A498-RAD10 cells were cross-resistant to cabozantinib, the tyrosine kinase inhibitor used in first-line treatment of mRCC with nivolumab...In silico data supported a context‑dependent role of PBRM1 in ccRCC patients. To the best of our knowledge, this is the first description of a mechanism of RAD001 and cabozantinib resistance through PBRM1 overexpression and CXCR7/CXCR4 downregulation and suggest new therapeutic perspective for cabozantinib-resistant patients.