Book contents
- Frontmatter
- Contents
- Contributors
- Overview: Biology Is the Foundation of Therapy
- PART I BASIC RESEARCH
- Introduction to Basic Research
- MODELS AND TOOLS FOR METASTASIS STUDIES
- GENES
- VARIOUS PROPERTIES OF CANCER CELLS
- STROMAL CELLS/EXTRACELLULAR MATRIX
- SYSTEMIC FACTORS
- 18 Exploring the Earliest Steps in Metastasis: The Pre-metastatic Niche
- 19 Growth Regulatory Pathways Contributing to Organ Selectivity of Metastasis
- 20 Determinants of Organ-Specific Metastasis
- 21 Function and Expression of the uPA/uPAR System in Cancer Metastasis
- 22 The Lymphatics: On the Route to Cancer Metastasis
- PART II CLINICAL RESEARCH
- Index
- References
21 - Function and Expression of the uPA/uPAR System in Cancer Metastasis
from SYSTEMIC FACTORS
Published online by Cambridge University Press: 05 June 2012
- Frontmatter
- Contents
- Contributors
- Overview: Biology Is the Foundation of Therapy
- PART I BASIC RESEARCH
- Introduction to Basic Research
- MODELS AND TOOLS FOR METASTASIS STUDIES
- GENES
- VARIOUS PROPERTIES OF CANCER CELLS
- STROMAL CELLS/EXTRACELLULAR MATRIX
- SYSTEMIC FACTORS
- 18 Exploring the Earliest Steps in Metastasis: The Pre-metastatic Niche
- 19 Growth Regulatory Pathways Contributing to Organ Selectivity of Metastasis
- 20 Determinants of Organ-Specific Metastasis
- 21 Function and Expression of the uPA/uPAR System in Cancer Metastasis
- 22 The Lymphatics: On the Route to Cancer Metastasis
- PART II CLINICAL RESEARCH
- Index
- References
Summary
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.
- Type
- Chapter
- Information
- Cancer MetastasisBiologic Basis and Therapeutics, pp. 223 - 236Publisher: Cambridge University PressPrint publication year: 2011
References
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