Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 39, Issue 4, Pages 183-190Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2014.02.006
Keywords
PTEN; PTEN-Long; PI3K signaling
Categories
Funding
- NCI NIH HHS [P01 CA097403, R01 CA184016, R01 CA082783, R01 CA155117] Funding Source: Medline
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Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a phosphatase that is frequently altered in cancer. PTEN has phosphatase-dependent and -independent roles, and genetic alterations in PTEN lead to deregulation of protein synthesis, the cell cycle, migration, growth, DNA repair, and survival signaling. PTEN localization, stability, conformation, and phosphatase activity are controlled by an array of protein-protein interactions and post-translational modifications. Thus, PTEN-interacting and -modifying proteins have profound effects on the tumor suppressive functions of PTEN. Moreover, recent studies identified mechanisms by which PTEN can exit cells, via either exosomal export or secretion, and act on neighboring cells. This review focuses on modes of PTEN protein regulation and ways in which perturbations in this regulation may lead to disease.
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