{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9(28)"],"submitter":["Kim EJ"],"pubmed_abstract":["Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. When compared to wild type SNU-C5 cells (WT), SNU-C5/5-FU cells showed over-activation of PI3K/AKT pathway, like increased phosphorylation of AKT, mTOR, and GSK-3β, nuclear localization of β-catenin, and decreased E-cadherin. Moreover, E-cadherin level was down-regulated in recurrent colon cancer tissues compared to primary colon cancer tissues. Gene silencing of AKT1 or treatment of LY294002 (PI3 kinase inhibitor) increased E-cadherin, whereas decreased phospho-GSK-3β. LY294002 also reduced protein level of β-catenin with no influence on mRNA level. PTEN level was higher in SNU-C5/WT than SNU-C5/5-FU cells, wher"],"journal":["Oncotarget"],"pagination":["19911-19928"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5929436"],"repository":["biostudies-literature"],"pubmed_title":["Over-activation of AKT signaling leading to 5-Fluorouracil resistance in SNU-C5/5-FU cells."],"pmcid":["PMC5929436"],"pubmed_authors":["Kang GJ","Kang HK","Kim EJ","Kang JI","Maeng YH","Kwon JM","Boo HJ","Koh YS","Lee CH","Chang WY","Yoo ES","Hyun JW","Kim YR"],"additional_accession":[]},"is_claimable":false,"name":"Over-activation of AKT signaling leading to 5-Fluorouracil resistance in SNU-C5/5-FU cells.","description":"Here, we investigated whether over-activation of AKT pathway is important in the resistance to 5-fluorouracil (5-FU) in SNU-C5/5-FU cells, 5-FU-resistant human colon cancer cells. When compared to wild type SNU-C5 cells (WT), SNU-C5/5-FU cells showed over-activation of PI3K/AKT pathway, like increased phosphorylation of AKT, mTOR, and GSK-3β, nuclear localization of β-catenin, and decreased E-cadherin. Moreover, E-cadherin level was down-regulated in recurrent colon cancer tissues compared to primary colon cancer tissues. Gene silencing of AKT1 or treatment of LY294002 (PI3 kinase inhibitor) increased E-cadherin, whereas decreased phospho-GSK-3β. LY294002 also reduced protein level of β-catenin with no influence on mRNA level. PTEN level was higher in SNU-C5/WT than SNU-C5/5-FU cells, wher","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Apr","modification":"2025-05-18T13:46:43.793Z","creation":"2025-05-18T13:46:43.793Z"},"accession":"S-EPMC5929436","cross_references":{"pubmed":["29731993"],"doi":["10.18632/oncotarget.24952"]}}