LAUSR

Background/Aim: Kindlins are essential integrin activators. Kindlin-1 and kindlin-2 are often concomitantly expressed in epithelial tumor cells and participate in regulating tumor malignancy. However, it remains unclear whether kindlin-3, the one expressed in immune cells, also plays a role in regulating tumor malignancy. Materials and Methods: To examine the role of kindlin-3 in different immune cells in regulating solid tumor growth, a xenograft model of prostate cancer tumor growth in genetically modified kindlin-3 mice was employed. Results: Disruption of crosstalk between kindlin-3 and integrins significantly promoted subcutaneous prostate cancer tumor growth in mice. Furthermore, deficiency of kindlin-3 in T cells and NK cells, but not myeloid cells and B cells, significantly enhanced prostate cancer tumor growth. Conclusion: Tumor-killing leukocytes require Kindlin-3 for suppressing cancerous tumor growth, thus providing a novel anticancer mechanism.