| Literature DB >> 30250923 |
Vaishali Jayashankar1, Brendan T Finicle1, Aimee L Edinger1.
Abstract
Our recent work demonstrates that inactivating mutations in phosphatase and tensin homolog (PTEN) are sufficient to drive macropinocytosis in the context of AMP-activated protein kinase (AMPK) activation. Given that blocking macropinocytosis limits PTEN-deficient prostate tumor growth, AMPK or phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) inhibitors could have therapeutic value in castration-resistant prostate cancer patients, particularly when used in combination with standard of care therapies. Abbreviations: ATG5: autophagy related 5; NHE: Na(+)/H(+) exchanger; PAK1: p21-activated kinase 1; PI3K: phosphatidylinositol-4,5-bisphosphate 3-kinase; PIP3: phosphatidylinositol (3,4,5)-trisphosphate; PIP2: phosphatidylinositol (4,5)-bisphosphate; RAC1: Rac family small GTPase 1.Entities:
Keywords: AMPK; PI3K pathway; PTEN; macropinocytosis; necrosis; nutrient scavenging; prostate cancer
Year: 2018 PMID: 30250923 PMCID: PMC6149707 DOI: 10.1080/23723556.2018.1472060
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556