The role of osteopontin in tumor metastasis

PY Wai, PC Kuo - Journal of Surgical Research, 2004 - Elsevier
PY Wai, PC Kuo
Journal of Surgical Research, 2004Elsevier
Osteopontin (OPN) is a glyco-phosphoprotein that is expressed and secreted by numerous
human cancers. OPN functions in cell adhesion, chemotaxis, macrophage-directed
interleukin-10 (IL-10) suppression, stress-dependent angiogenesis, prevention of apoptosis,
and anchorage-independent growth of tumor cells by regulating cell-matrix interactions and
cellular signaling through binding with integrin and CD44 receptors. While constitutive
expression of OPN exists in several cell types, induced expression has been detected in T …
Osteopontin (OPN) is a glyco-phosphoprotein that is expressed and secreted by numerous human cancers. OPN functions in cell adhesion, chemotaxis, macrophage-directed interleukin-10 (IL-10) suppression, stress-dependent angiogenesis, prevention of apoptosis, and anchorage-independent growth of tumor cells by regulating cell-matrix interactions and cellular signaling through binding with integrin and CD44 receptors. While constitutive expression of OPN exists in several cell types, induced expression has been detected in T-lymphocytes, epidermal cells, bone cells, macrophages, and tumor cells in remodeling processes such as inflammation, ischemia-reperfusion, bone resorption, and tumor progression. Recently, substantial evidence has linked OPN with the regulation of metastatic spread by tumor cells. However, the molecular mechanisms that define the role of OPN in tumor metastasis are incompletely understood. Transcriptional regulators that contribute to the induction of OPN expression have received significant attention as potential modulators of the OPN-mediated metastatic phenotype. The following review will discuss the molecular structure of OPN, the evidence for its functional role in tumor cell metastasis, the downstream signals that activate invasive mechanisms, and the recent reports concerning regulation of OPN transcription.
Elsevier