Abstract
Endothelin 1 (ET-1) is produced by several types of human cancer cells and has been proposed to participate in tumor development or progression by exerting autocrine or paracrine actions on neoplastic cells and their surrounding stromal cells. Recently, an ET-1-mediated autocrine loop has been implicated in the growth of ovarian tumor cells. The co-expression of ET-1 and ET A receptors, with consequent activation of growth signaling pathways in human ovarian carcinoma cells, constitutes a mechanism for the autocrine regulation of tumor cell growth. Such findings also provide a basis for further investigation of the role of tyrosine phosphorylation in ET-1-regulated growth responses in ovarian tumor cells. The overexpression of ET-1 and its receptor in cancer cells may serve as a tumor marker, and could provide potential targets for therapy.
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.
