Platelet and neutrophil cross-talk-mediating cancer growth and metastasis in patients with urinary bladder cancer

الملخص EN

Background / Aim : The initial selectin-dependent events that mediate tumor cell tethering to platelets, leukocytes, and vascular endothelium can regulate the extravasation and colonization of metastatic cells into distant tissues.

We aimed to clarify the role of selectin–selectin ligand interactions in tumor growth and progression in patients with bladder cancer.

Patients and methods Thirty patients with bladder cancer were the participants in this study classified as follows: locally invasive group (n = 10), urinary bladder cancer group with regional lymph node involvement (n = 10), and urinary bladder cancer group with regional lymph nodes and distant metastasis (n = 10).

Flow cytometry was used to determine both the platelet surface expression of P-selectin (CD62P) and the neutrophil surface expression of PSGL-1 (CD162), whereas enzyme-linked immunosorbent assay was used for the assay of soluble P-selectin.

Results Neutrophil PSGL-1 expression among the different groups studied was not statistically significant.

However, there was enhanced platelet activation as evidenced by increased platelet surface expression of P-selectin together with an increase in its soluble form, which was more prominent with advancement of the disease, especially in patients with distant metastasis.

Also, a strong positive correlation was found between platelet P-selectin and its soluble form with the tumor grading.

In addition, stepwise multiple regression analysis showed that both P-selectin and platelet count are significant independent determinants for the stage of bladder cancer, suggesting augmentation of P-selectin–ligand interaction.

Conclusion These data preclude that disease progression in patients with bladder cancer is dependent on the complex interaction between P-selectin and its ligand.

Targeting of these molecules may represent a unique approach to tumor therapy and prevention of metastasis.