{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(5)"],"submitter":["Bar N"],"pubmed_abstract":["<h4>Background</h4>The tumor suppressor PTEN (phosphatase and tensin homolog) is a lipid phosphatase that converts PIP3 into PIP2 and downregulates the kinase AKT and its proliferative and anti-apoptotic activities. The FoxO transcription factors are PTEN downstream effectors whose activity is negatively regulated by AKT-mediated phosphorylation. PTEN activity is frequently lost in many types of cancer, leading to increased cell survival and cell cycle progression.<h4>Principal findings</h4>Here we characterize the widely expressed miR-22 and report that miR-22 is a novel regulatory molecule in the PTEN/AKT pathway. miR-22 downregulates PTEN levels acting directly through a specific site on PTEN 3'UTR. Interestingly, miR-22 itself is upregulated by AKT, suggesting that miR-22 forms a feed-forward circuit in this pathway. Time-resolved live imaging of AKT-dependent FoxO1 phosphorylation revealed that miR-22 accelerated AKT activity upon growth factor stimulation, and attenuated its down regulation by serum withdrawal.<h4>Conclusions</h4>Our results suggest that miR-22 acts to fine-tune the dynamics of PTEN/AKT/FoxO1 pathway."],"journal":["PloS one"],"pagination":["e10859"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2877705"],"repository":["biostudies-literature"],"pubmed_title":["miR-22 forms a regulatory loop in PTEN/AKT pathway and modulates signaling kinetics."],"pmcid":["PMC2877705"],"pubmed_authors":["Dikstein R","Bar N"],"additional_accession":[]},"is_claimable":false,"name":"miR-22 forms a regulatory loop in PTEN/AKT pathway and modulates signaling kinetics.","description":"<h4>Background</h4>The tumor suppressor PTEN (phosphatase and tensin homolog) is a lipid phosphatase that converts PIP3 into PIP2 and downregulates the kinase AKT and its proliferative and anti-apoptotic activities. The FoxO transcription factors are PTEN downstream effectors whose activity is negatively regulated by AKT-mediated phosphorylation. PTEN activity is frequently lost in many types of cancer, leading to increased cell survival and cell cycle progression.<h4>Principal findings</h4>Here we characterize the widely expressed miR-22 and report that miR-22 is a novel regulatory molecule in the PTEN/AKT pathway. miR-22 downregulates PTEN levels acting directly through a specific site on PTEN 3'UTR. Interestingly, miR-22 itself is upregulated by AKT, suggesting that miR-22 forms a feed-forward circuit in this pathway. Time-resolved live imaging of AKT-dependent FoxO1 phosphorylation revealed that miR-22 accelerated AKT activity upon growth factor stimulation, and attenuated its down regulation by serum withdrawal.<h4>Conclusions</h4>Our results suggest that miR-22 acts to fine-tune the dynamics of PTEN/AKT/FoxO1 pathway.","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 May","modification":"2021-03-07T08:35:15Z","creation":"2019-03-26T23:07:32Z"},"accession":"S-EPMC2877705","cross_references":{"pubmed":["20523723"],"doi":["10.1371/journal.pone.0010859"]}}