We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure coreplatform@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Metastatic disease is responsible for most cancer lethality; therefore, understanding the intricate interplay among tumor cells, soluble factors, extracellular matrix (ECM), and host cells during cancer progression to metastasis is crucial to designing successful therapies [1]. Metastasis is formed when a cell, or a group of cells, leaves the original site of the primary tumor and establishes a new colony of tumor cells in a distant, anatomically separate, site in the body [1]. To form an overt metastasis, the cells must overcome the regulatory and physical constraints imposed by the tissue milieu and initiate proliferation and invasive growth. Proteases and their inhibitors and receptors, such as those that comprise the urokinase-type plasminogen activator (uPA) system, play a crucial role in determining the ability of tumor cells to metastasize (Figure 21.1). Interestingly, dissemination of tumor cells and metastatic growth promoted by uPA and its receptor (uPAR) may be caused not only by proteolysis but also by novel functions related to cell signaling necessary for tumor cells to migrate, survive, and proliferate in target organs [1, 2]. The role of uPAR in regulating cell motility, which appears to operate similarly in normal and tumor cells, has been covered recently in extensive reviews [3]. This chapter focuses on recent advances that focus on how the uPA system coordinates proteolysis and signal transduction for invasion, dissemination, survival, and mitogenesis during tumor progression.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.