| Literature DB >> 31932468 |
Larissa Kotelevets1,2, Barbara Trifault3,4,5, Eric Chastre1,2, Mark G H Scott3,4,5.
Abstract
Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor that is frequently down-modulated in human cancer. PTEN inhibits the phosphatidylinositol 3-phosphate kinase (PI3K)/AKT pathway through its lipid phosphatase activity. Multiple PI3K/AKT-independent actions of PTEN, protein-phosphatase activities and functions within the nucleus have also been described. PTEN, therefore, regulates many cellular processes including cell proliferation, survival, genomic integrity, polarity, migration, and invasion. Even a modest decrease in the functional dose of PTEN may promote cancer development. Understanding the molecular and cellular mechanisms that regulate PTEN protein levels and function, and how these may go awry in cancer contexts, is, therefore, key to fully understanding the role of PTEN in tumorigenesis. Here, we discuss current knowledge on posttranslational control and conformational plasticity of PTEN, as well as therapeutic possibilities toward reestablishment of PTEN tumor-suppressor activity in cancer.Entities:
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Year: 2020 PMID: 31932468 PMCID: PMC7328454 DOI: 10.1101/cshperspect.a036095
Source DB: PubMed Journal: Cold Spring Harb Perspect Med ISSN: 2157-1422 Impact factor: 5.159