In conclusion, bortezomib may induce ERK phosphorylation to suppress cathepsin B and inhibit the catalytic process of autophagy in ovarian cancer and other solid tumors.
Inhibition of protease activity by the cysteine protease inhibitor, E-64, and treatment of ovarian cancer cells with small interfering RNA against cathepsin B suppressed the ability of tumor-shed microvesicles to stimulate both gelatinase activation and the invasiveness of endothelial cells observed at low pH values.
The presented results suggest that cathepsin B and its interacting proteins, bikunin and TSRC1, are involved in the apoptotic pathway of ovarian cancer cells.
Accordingly, cathepsin B can be regarded as unfavorable and as an independent tumor marker for progression-free survival and overall survival in ovarian cancer patients with long follow-up.