<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(28)</volume><submitter>Kim EJ</submitter><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</pubmed_abstract><journal>Oncotarget</journal><pagination>19911-19928</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5929436</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Over-activation of AKT signaling leading to 5-Fluorouracil resistance in SNU-C5/5-FU cells.</pubmed_title><pmcid>PMC5929436</pmcid><pubmed_authors>Kang GJ</pubmed_authors><pubmed_authors>Kang HK</pubmed_authors><pubmed_authors>Kim EJ</pubmed_authors><pubmed_authors>Kang JI</pubmed_authors><pubmed_authors>Maeng YH</pubmed_authors><pubmed_authors>Kwon JM</pubmed_authors><pubmed_authors>Boo HJ</pubmed_authors><pubmed_authors>Koh YS</pubmed_authors><pubmed_authors>Lee CH</pubmed_authors><pubmed_authors>Chang WY</pubmed_authors><pubmed_authors>Yoo ES</pubmed_authors><pubmed_authors>Hyun JW</pubmed_authors><pubmed_authors>Kim YR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Over-activation of AKT signaling leading to 5-Fluorouracil resistance in SNU-C5/5-FU cells.</name><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</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Apr</publication><modification>2025-05-18T13:46:43.793Z</modification><creation>2025-05-18T13:46:43.793Z</creation></dates><accession>S-EPMC5929436</accession><cross_references><pubmed>29731993</pubmed><doi>10.18632/oncotarget.24952</doi></cross_references></HashMap>