NGFR overexpression

In surgically resected specimens, pERK, a known player in proliferation signaling, colocalizes with CD271. These data indicate that CD271 is involved in bladder cancer malignancy by promoting cell proliferation and migration, resulting in poor prognosis.

Our study provides evidence that CD271 could prevent the switch between low to high-risk cSCC tumors. Because CD271 contributes to maintaining active differentiative paths and favors the response to therapies, it might be a promising target for future pharmaceutical development.

The grafting of CD271-overexpressing cells resulted in a significantly lower metastatic capacity and promoted the recruitment of macrophages within the site of injection. Therefore, our results indicate an inverse correlation between CD271 expression and malignancy level and CD271 could potentially have a role in the switch between the less aggressive to the high-risk cSCC

Therefore, we postulate that NGFR could modify immune cell recognition to generate immunosuppressive environments that favour tumour metastasis. Conclusion Overall, our data suggest that combination of immunotherapy with NGFR inhibition could improve melanoma treatment by targeting tumour metastasis and overcoming resistance to immunotherapy.

Finally, CD271 upregulation inhibited mROS production, revealing the presence of a negative feedback loop in mROS regulation. These results indicate that targeting CD271 can activate cell death pathways to inhibit melanoma progression and potentially overcome resistance to targeted therapy.

Five-year overall and disease-free survival in NGFR+/S100A9+ patients was better than in NGFR-/S100A9- patients. This study's findings suggest that NGFR may serve as a marker predicting CRC patients' chemosensitivity.