FPR3 (Formyl Peptide Receptor 3)

Moreover, FPR3 silencing also impeded nuclear translocation of β-catenin, thereby suppressing canonical Wnt/β-catenin signaling and the expressions of proteins associated with EMT. Taken together, our data elucidate the clinical value and function of FPR3 in immune suppression and Wnt/β-catenin pathway activation, suggesting that FPR3 may be a novel therapeutic target for interventions against colon adenocarcinoma metastasis.

Notably, Sig27IMG stratified patients with a poor prognosis risk in these 17 cancer types. In summary, Sig27 and its derivative panel, Sig27IMG, offer a robust assessment of PC recurrence, highlighting immunosuppressive features mediated by TAMs, dendritic cells, and endothelial cells across multiple cancer types.

These findings underscore the profound infiltration of FPR3 + macrophages in breast cancer patients with adverse prognoses, highlighting FPR3 as a potential therapeutic target for intervening breast cancer aggressiveness.

Inhibition of MMP1 in vitro demonstrated reduced cell invasion, stemness, and proliferation, while increasing reactive oxygen species levels and promoting apoptosis. Our findings position MMP1 as a key player in the "tumor-immune" vicious cycle and a promising therapeutic target to enhance anti-tumor responses and improve patient outcomes.

Based on Perturb-seq and functional investigations, GPR183 also enhances effector functions, such that engineering NK and CAR NK cells to express GPR183 enhances their ability to migrate to, infiltrate, and control breast cancer tumors. Our study uncovered metabolite-based tumor immune recruitment mechanisms, opening avenues for spatially targeted cell therapies.

Sig27 is a novel and effective pan-RCC biomarker with high-level associations with RCC immunosuppressive features.

p-ERK5 and p-AKT in breast cancer cells was significantly reduced after FPRL2 knocked down. In Conclusion, FPRL2 mediates Adriamycin resistance in breast cancer cells, and knockdown of FPRL2 increased apoptosis and decreased Adriamycin resistance in breast cancer cells.

The potential biological relevance of FPR3 was confirmed in glioma, and it was shown to have significant involvement in the processes of glioma growth, immune infiltration, and metastasis. Our results imply a potential association of FPR3 with tumor immunity, indicating its viability as a prognostic indicator in glioma.

The risk score of this model consistently and effectively predicted overall survival, surpassing the accuracy of conventional clinical factors and 100 previously published signatures. Consequently, the CD163+FPR3+ macrophage-related score shows potential as a prognostic biomarker for glioma patients.

Immunohistochemical results confirmed that C1QB, FCER1G, FPR3 and TYROBP were significantly associated with disease progression in GC. Our study identified that C1QB, FCER1G, FPR3 and TYROBP played important roles in the progression of GC, and their specific mechanisms are worth further study.

Furthermore, miR-6839-5p inhibitor can restore or partially restore the expression value of the above four genes. The analysis results of miRNA target gene prediction database indicated VEGFA was the most likely direct target gene of miR-6839-5p.

Additionally, NFATc1 directly binds to the sex determining region Y-box 2 (SOX2) promoter and modifies stemness in GC. In conclusion, our work illustrated that FPR3 played a negative role in GC progression by modulating NFATc1-mediated glycolysis and stemness in a calcium-dependent manner, providing potential insights into cancer therapy.