Adipocytes are a known source of stem cells. They are easy to harvest, and are a suitable candidate for autogenous grafts. Adipose derived stem cells (ADSCs) have multiple target tissues which they can differentiate into, including bone and cartilage. In adipose tissue, ADSCs are able to differentiate, as well as providing energy and a supply of cytokines/hormones to manage the hypoxic and lipid/hormone saturated adipose environment. The plasminogen activation system (PAS) controls the majority of proteolytic activities in both adipose and wound healing environments, allowing for rapid cellular migration and tissue remodelling. While the primary activation pathway for PAS occurs through the urokinase plasminogen activator (uPA), which is highly expressed by endothelial cells, its function is not limited to enabling revascularisation. Proteolytic activity is dependent on protease activation, localisation, recycling mechanisms and substrate availability. uPA and uPA activated plasminogen allows pluripotent cells to arrive to new local environments and fulfil the niche demands. However, overstimulation, the acquisition of a migratory phenotype and constant protein turnover can be unconducive to the formation of structured hard and soft tissues. To maintain a suitable healing pattern, the proteolytic activity stimulated by uPA is modulated by plasminogen activator inhibitor 1. Depending on the physiological settings, different parts of the remodelling mechanism are activated with varying results. Utilising the differences within each microenvironment to recreate a desired niche is a valid therapeutic bio-engineering approach. By controlling the rate of protein turnover combined with a receptive stem cell lineage, such as ADSC, a novel avenue on the therapeutic opportunities may be identified, which can overcome limitations, such as scarcity of stem cells, low angiogenic potential or poor host tissue adaptation.

Soy isoflavones are dietary components for which an association has been demonstrated with reduced risk of prostate cancer (PCa) in Asian populations. However, the exact mechanism by which these isoflavones may prevent the development or progression of PCa is not completely understood. There are a growing number of animal and in vitro studies that have attempted to elucidate these mechanisms. The predominant and most biologically active isoflavones in soy products, genistein, daidzein, equol, and glycetin, inhibit prostate carcinogenesis in some animal models. Cell-based studies show that soy isoflavones regulate genes that control cell cycle and apoptosis. In this review, we discuss the literature relevant to the molecular events that may account for the benefit of soy isoflavones in PCa prevention or treatment. These reports show that although soy isoflavone-induced growth arrest and apoptosis of PCa cells are plausible mechanisms, other chemo protective mechanisms are also worthy of consideration. These possible mechanisms include antioxidant defense, DNA repair, inhibition of angiogenesis and metastasis, potentiation of radio- and chemotherapeutic agents, and antagonism of estrogen- and androgen-mediated signaling pathways. Moreover, other cells in the cancer milieu, such as the fibroblastic stromal cells, endothelial cells, and immune cells, may be targeted by soy isoflavones, which may contribute to soy-mediated prostate cancer prevention. In this review, these mechanisms are discussed along with considerations about the doses and the preclinical models that have been used.