A number of reports have shown that OPG is known as a survival component which could block TRAIL induced apoptosis in tumor cells. Human prostate cancer cells had been proven to secrete OPG at concentrations ample to inhibit TRAIL induced apoptosis in vitro Similarly, multiple myeloma cells were protected from TRAIL induced apoptosis by OPG secreted from osteoblast like cells and bone marrow stroma cells OPG selleck chemicals created by breast cancer cells en hances tumor cell survival in vitro and in vivo by inhibit ing TRAIL induced apoptosis The production of OPG in colorectal cancer cells along with the addition of exogen ous OPG to colorectal cancer cells the two induced resistance to TRAIL induced apoptosis Exogenous addition of OPG also mediates resistance to TRAIL induced apoptosis in ovarian cancer cells Since OPG binds to TRAIL, more hints OPG mediated protection from TRAIL in various cancer cells continues to be assumed to be mainly associated to its decoy perform.
Yet, the observations that OPG activates integrin focal adhesion kinase ERKl 2 signaling in endothelial cells to advertise proliferation and migration propose that OPG regulates cell function immediately. Certainly, it was advised that OPG mediated proliferation and migration of endothelial cells occurs in the TRAIL independent method In ovarian cancer cells, activation of integrin FAK and ERI l 2 signaling contribute to attenuate TRAIL induced apoptosis Dependant on these observations, we hypothesize that OPG may attenuate TRAIL induced apoptosis in a TRAIL binding independent manner by activating survival signaling pathways in ovarian cancer cells. The objective of this review was to investigate whether or not exogenous OPG can confer safety towards TRAIL induced apoptosis inde pendent from its ability to act like a TRAIL decoy receptor.