Liu Anne, Zhu Yanyu, Chen Weiping, Merlino Glenn, Yu Yanlin
Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Cancers (Basel). 2022 Jul 28;14(15):3666. doi: 10.3390/cancers14153666.
PTEN is the second most highly mutated tumor suppressor in cancer, following only p53. The PTEN protein functions as a phosphatase with lipid- and protein-phosphatase activity. PTEN-lipid-phosphatase activity dephosphorylates PIP3 to form PIP2, and it then antagonizes PI3K and blocks the activation of AKT, while its protein-phosphatase activity dephosphorylates different protein substrates and plays various roles in tumorigenesis. Here, we review the PTEN mutations and protein-phosphatase substrates in tumorigenesis and metastasis. Our purpose is to clarify how PTEN protein phosphatase contributes to its tumor-suppressive functions through PI3K-independent activities.
PTEN是癌症中第二高突变的肿瘤抑制因子，仅次于p53。PTEN蛋白作为一种具有脂质和蛋白质磷酸酶活性的磷酸酶发挥作用。PTEN脂质磷酸酶活性使PIP3去磷酸化形成PIP2，然后拮抗PI3K并阻断AKT的激活，而其蛋白质磷酸酶活性使不同的蛋白质底物去磷酸化，并在肿瘤发生中发挥多种作用。在这里，我们综述了肿瘤发生和转移过程中的PTEN突变和蛋白质磷酸酶底物。我们的目的是阐明PTEN蛋白磷酸酶如何通过不依赖PI3K的活性促进其肿瘤抑制功能。
Zotero 插件
