CXCR2 (Chemokine (C-X-C motif) receptor 2)

P=N/A, N=48, Recruiting, Duke University | Trial completion date: Oct 2026 --> Jan 2028 | Trial primary completion date: Jan 2026 --> Jul 2027

SH may exert its anti-PCa effects by regulating key biomarkers such as GSTP1 and CXCR2, interfering with oncogenic signalling pathways including Rap1, Ras and MAPK, and modulating the infiltration levels of immune cells such as M0/M1 macrophages simultaneously. The online version contains supplementary material available at 10.1007/s40203-025-00511-5.

Furthermore, Cx2Mab-5 detected mCXCR2 in Western blot and immunohistochemistry in CHO/mCXCR2 cells, but a commercially available anti-mCXCR2 mAb (clone SA045E1) did not. Hence, Cx2Mab-5 can be a valuable tool for analyzing mCXCR2-positive cells in mouse tissues.

We show that these effects depend on the CXCL5/CXCR2 signalling axis. Taken together, we demonstrate that osteoblasts enhance cancer growth in a bone metastatic niche and that this effect is reversible with CXCL5/CXCR2 inhibition.

These findings highlight a central role for CXCR2-mediated signaling in the development of radioresistance in HPV-negative HNSCC cells.

Mechanistically, UVB modulates the tumor immune environment: Mass cytometry of CD45+ immune infiltrate cells from lung metastases of mice UVB-and sham-irradiated revealed a UVB-induced increase in CXCR2- neutrophils and a reduction in Ly6C+ inflammatory monocytes, with no changes in regulatory T cells or expression of immune checkpoint molecules. Together, these results highlight a potentially protective role of UVB and solar radiation and provide a rationale for further investigation into UV as a factor that enhances antitumor immunity.

Inhibition of SREBP2, pharmacological blockade of CXCL1, or perturbation of NETs markedly reduced PDAC growth in diabetic mouse models. Together, these multi-omics analyses and follow-up mechanistic studies constitute an integrated approach that elucidates a metabolic mechanism by which diabetes promotes PDAC development by remodeling the tumor immune microenvironment and highlights a potential therapeutic strategy for PDAC with DM.

The existing in vitro evidence suggests that mesenchymal stem cells may exhibit a potential to promote EMT in HNSCC, potentially regulating tumor progression through multiple signaling pathway networks and providing new potential targets for future therapies targeting the TME. However, more high-quality, standardized in vivo and in vitro studies are needed to further validate the related mechanisms and therapeutic potential.

AKR1B10 facilitated immune evasion of KRASG12C mutation CRLM by recruiting and reprogramming neutrophils to remodel the immunosuppressive TME, providing a potential therapeutic target for KRASG12C mutation CRLM patients.

Our data point to Cxcr2 as a critical and multifunctional regulator of healthy bone homeostasis, linking immune function with skeletal integrity. This work highlights the Cxcr2 KO model as a valuable system for studying inflammatory bone loss and osteoimmunological interactions.

Chlorogenic acid acts as a promising multi-target ligand in CRC prevention, with our in silico evidence supporting its ability to modulate diverse oncogenic pathways. Further experimental studies are warranted to confirm its efficacy and translational potential.

There is a significant association between CXCL5/CXCR2 and UC under the MR assumption, which is potentially linked with colonic chemotaxis and activation of neutrophils. These findings highlight the potential of CXCL5/CXCR2 as a therapeutic target for UC. However, future functional studies are needed to validate these findings and explore the exact mechanisms by which CXCL5/CXCR2 influences immune cell crosstalk in UC.