Endometriosis (EM) is a disease that involves active endometrial cell invasion and migration which is an important reason for
infertility. Anoikis resistance is the most important prerequisite for EM, but the molecular mechanism is not yet clear.
Kallistatin (KS) is one kind of
serine protease inhibitors which had extensive biological function including anti-inflammatory,
antioxidant stress, anti-angiogenesis, and anti-
tumor. Our preliminary data showed that the level of KS in EM patients' endometrial tissue and blood were much lower than control (non-EM) patients without
endometriosis. Interestingly, the decrease of KS is correlated with the severity of
endometriosis. Moreover,
kallistatin recombinant protein could increase the anoikis rate of ectopic endometrium cells (EESCs), and then inhibits its
metastasis and invasion. Mechanically, our data show that the EESCs have lower intracellular
reactive oxygen species (ROS) production and KS can elevate the ROS levels significantly. Further, KS modulate expression of MnSOD and
caspase 3 signaling in EESCs grown in suspended conditions. These findings reveal novel mechanisms of KS in inducing anoikis and
metastasis in EESCs, thus inhibiting EM progression by regulation of MnSOD and
caspase 3 signaling. Our findings suggest that KS is a significant
protein with prospects for application in EM.