Procathepsin D and cancer: From molecular biology to clinical applications

Figure 1 Level of anti-procathepsin D autoantibodies in patients with three types of cancer and two cancer-unrelated diseases evaluated by enzyme-linked immunosorbent assay. Data represent mean value from 5 patients/group.

Figure 2 Level of anti-procathepsin D autoantibodies in patients with various stages of breast cancer evaluated by enzyme-linked immunosorbent assay. Average age of patients in each group varied from 31 to 69.

Figure 3 Proposed mechanism of procathepsin D/cathepsin D function in cancer progression. The over-expressed procathepsin D (pCD) escapes the physiological intracellular targeting pathways and is secreted by the cancer cells. Small part of secreted pCD is bound and internalized via M6PR pathway, the rest by a yet unidentified receptor. The receptor-pCD interaction activates mitogen-activated protein kinases (MAPK) pathway with subsequent changes in expression of numerous cancer-promoting genes including NFKB2 and some cytokines. Interaction of pCD with endothelial and stromal cells is also involved.

Figure 4 Stress affects keratinocytes resulting in increased both cytokine and procathepsin D synthesis and secretion leading to the elevated proliferation of keratinocytes.