Akt/PKB signaling in cancer: a function in cell motility and invasion.
The PI 3-K signaling pathway has been the subject of intense investigation for over a decade because it regulates a multitude of cellular processes. Deregulation of this pathway often results in human diseases such as cancer. The serine/threonine kinase Akt, a major PI 3-K target in all cells, has received considerable attention because it provides tumor cells with enhanced survival capacity. Many tumors and tumor cells display elevated Akt protein expression and activity, and many of the proteins which regulate Akt itself are also often mutated in cancer. For this reason, Akt has become a viable drug target for cancer therapy. However, recent studies have shown that Akt can also function as a suppressor of tumor cell migration and invasion, phenotypes which are directly linked to metastatic tumor progression. Here we review these findings and consider the unexpected notion that Akt may function as a metastasis suppressor.
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
Merav
M
Yoeli-Lerner
Alex
A
Toker
D000818:Animals; D002465:Cell Movement / Q000235:genetics*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D009361:Neoplasm Invasiveness / Q000235:genetics*; D009362:Neoplasm Metastasis / Q000235:genetics*; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
D025521:Tumor Suppressor Proteins; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases