<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Michel M</submitter><pubmed_abstract>Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis. Overexpression of Glo-I has been linked to multi-drug resistance in cancer therapy. The aim of this study was to analyze Glo-I in hepatocellular carcinoma (HCC) and the effect of the multi-tyrosine kinase inhibitor sorafenib on Glo-I. Methods: Expression and specific activity of Glo-I was measured in human HCC samples, HCC-cell lines (HepG2, Huh7) and a hepatocyte cell line (AML 12). Cells were either treated with Glo-I inhibitors, ethyl pyruvate (EP, 1-20 mM) and BrBzGSHCp2 (1-10 μM), or sorafenib (2.5-10 μM) and protein expression (Western Blot), proliferation (WST-assay), migration (scratch assay), and colony formation (clonogenic assay) were assessed. Results: High expres</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>785</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6710403</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Inhibition of Glyoxalase-I Leads to Reduced Proliferation, Migration and Colony Formation, and Enhanced Susceptibility to Sorafenib in Hepatocellular Carcinoma.</pubmed_title><pmcid>PMC6710403</pmcid><pubmed_authors>Zipprich A</pubmed_authors><pubmed_authors>Michel M</pubmed_authors><pubmed_authors>Ripoll C</pubmed_authors><pubmed_authors>Pohl S</pubmed_authors><pubmed_authors>Hollenbach M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of Glyoxalase-I Leads to Reduced Proliferation, Migration and Colony Formation, and Enhanced Susceptibility to Sorafenib in Hepatocellular Carcinoma.</name><description>Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis. Overexpression of Glo-I has been linked to multi-drug resistance in cancer therapy. The aim of this study was to analyze Glo-I in hepatocellular carcinoma (HCC) and the effect of the multi-tyrosine kinase inhibitor sorafenib on Glo-I. Methods: Expression and specific activity of Glo-I was measured in human HCC samples, HCC-cell lines (HepG2, Huh7) and a hepatocyte cell line (AML 12). Cells were either treated with Glo-I inhibitors, ethyl pyruvate (EP, 1-20 mM) and BrBzGSHCp2 (1-10 μM), or sorafenib (2.5-10 μM) and protein expression (Western Blot), proliferation (WST-assay), migration (scratch assay), and colony formation (clonogenic assay) were assessed. Results: High expres</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2025-04-05T09:36:25.299Z</modification><creation>2019-09-07T07:01:28Z</creation></dates><accession>S-EPMC6710403</accession><cross_references><pubmed>31482070</pubmed><doi>10.3389/fonc.2019.00785</doi></cross_references></HashMap>