Abstract
Hepsin is required for the growth and maintenance of normal morphology, as well as for cell motility and development, initiation of blood coagulation and pro-inflammatory immune response. Here we showed that Cathepsin D (CtsD) as a novel protein is involved in the regulation of hepsin. CtsD destabilizes hepsin by promoting its ubiquitylation and subsequent proteasomal degradation in breast cancer cells. Breast cancer tissue microarray also indicated that hepsin expression was negatively correlated with CtsD by immunohistochemistry. Overexpression of CtsD promoted breast cancer cell migration, invasion and metastasis by enhancing the expression of intercellular cell adhesion molecule-1 (ICAM-1) in vitro and in vivo. These effects were inhibited by ectopic hepsin expression. Taken together, our data reveal a critical CtsD-hepsin signaling axis in migration and metastasis, which may contribute to a better understanding of the function and molecular mechanism in breast cancer progression.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
