In a cancer cell, proteolytic proenzymess have the effect of converting globular actin into tight filamentous actin, which causes the cancer cell structure to collapse and induce cell death. This reduces tumor volume and is often noticed in clinical practice.

Other mechanisms are thought to also contribute to the anticancer effects of proteolytic proenzymess, including inactivation of growth factors, which can often contribute to cancer cell growth. Data has been generated showing PRP also inhibits the growth of blood vessels. Scientific data published by Desser et al in 2001 has shown oral therapy with proteolytic enzymes decreases excessive TGF-beta (tumor growth factor) levels in human blood.

Additional effects, which have been observed, include triggering cell necrosis (cell death), induction of apoptosis (programmed cell death), the induction of cell differentiation (i.e. inducing cancer cells to exhibit more normal cell behavior), the inhibition of angiogenesis (preventing new blood vessel formation) in tumors, and anti-metastases (prevention of tumor spreading) by increasing adhesion between tumor cells.

PRP treatment regulates up to four relevant pathways related to cancer spread and metastasis, such as TGFβ, Hippo, Wnt and Notch pathways. In short, PRP treatment promotes the up-regulation of RAC1b which avoids the hyper-activation of the p38 pathway induced by the TGFβ pathway leading to the phosphorylation of YAP, which also explains the blockage of the canonical Wnt pathway, the inhibition of the Notch pathway as well as the cytoplasmic location of β−catenin in treated cells. That cascade of reactions implies the disruption of the CSC phenotype and the reversion of the malignant epithelial to mesenchymal transition process that lead to tumour invasion. In fact, PRP downregulation of TGFβ-1, had implications in tumour engraftment. In vivo experiments using a nude mice model, in which tumours were induced by inoculation of pancreatic CSCs, showed that PRP impaired CSCs subpopulation activation, niche formation and tumour initiation.

To have a wider view of PRP mode of action please read the scientific publication: Hernandez el at., Sci Rep. 2019 Aug 6;9(1):11359.