{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9"],"submitter":["Michel M"],"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"],"journal":["Frontiers in oncology"],"pagination":["785"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6710403"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of Glyoxalase-I Leads to Reduced Proliferation, Migration and Colony Formation, and Enhanced Susceptibility to Sorafenib in Hepatocellular Carcinoma."],"pmcid":["PMC6710403"],"pubmed_authors":["Zipprich A","Michel M","Ripoll C","Pohl S","Hollenbach M"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of Glyoxalase-I Leads to Reduced Proliferation, Migration and Colony Formation, and Enhanced Susceptibility to Sorafenib in Hepatocellular Carcinoma.","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","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019","modification":"2025-04-05T09:36:25.299Z","creation":"2019-09-07T07:01:28Z"},"accession":"S-EPMC6710403","cross_references":{"pubmed":["31482070"],"doi":["10.3389/fonc.2019.00785"]}}