0000000000289241

AUTHOR

Daekwan Seo

showing 4 related works from this author

MYC Activates Stem-like Cell Potential in Hepatocarcinoma by a p53-Dependent Mechanism

2014

Activation of c-MYC is an oncogenic hallmark of many cancers including liver cancer, and is associated with a variety of adverse prognostic characteristics. Despite a causative role during malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation for the biology of hepatic cancer stem cells (CSCs) are undefined. Here, distinct levels of c-MYC over-expression were established by using two dose-dependent tetracycline inducible systems in 4 hepatoma cell lines with different p53 mutational status. The CSCs were evaluated using side-population approach as well as standard in vitro and in vivo assays. Functional repression of p53 was achieved by lentivira…

Homeobox protein NANOGCancer ResearchCarcinoma HepatocellularCarcinogenesisMice SCIDBiologymedicine.disease_causeArticleMalignant transformationProto-Oncogene Proteins c-mycSide populationMice Inbred NODCancer stem cellmedicineAnimalsHumansLiver NeoplasmsHep G2 Cellsmedicine.diseaseTumor BurdenTransplantationPhenotypeOncologyImmunologyNeoplastic Stem CellsCancer researchTumor Suppressor Protein p53Liver cancerCarcinogenesisReprogrammingNeoplasm TransplantationCancer Research
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Loss of c-Met signaling sensitizes hepatocytes to lipotoxicity and induces cholestatic liver damage by aggravating oxidative stress.

2016

Recent studies confirmed a critical importance of c-Met signaling for liver regeneration by modulating redox balance. Here we used liver-specific conditional knockout mice (MetKO) and a nutritional model of hepatic steatosis to address the role of c-Met in cholesterol-mediated liver toxicity. Liver injury was assessed by histopathology and plasma enzymes levels. Global transcriptomic changes were examined by gene expression microarray, and key molecules involved in liver damage and lipid homeostasis were evaluated by Western blotting. Loss of c-Met signaling amplified the extent of liver injury in MetKO mice fed with high-cholesterol diet for 30days as evidenced by upregulation of liver enz…

0301 basic medicinemedicine.medical_specialtyCell SurvivalCholestasis IntrahepaticBiologyToxicologymedicine.disease_causeArticleCholesterol Dietary03 medical and health sciencesMice0302 clinical medicineLiver Function TestsInternal medicinemedicineAnimalsLiver X receptorLiver injuryMice Knockoutmedicine.diagnostic_testLipid metabolismProto-Oncogene Proteins c-metmedicine.diseaseLipid MetabolismGlutathioneLipidsLiver regenerationOxidative Stress030104 developmental biologyEndocrinologyLipotoxicity030220 oncology & carcinogenesisHepatocytesLipid PeroxidationSteatosisLiver function testsOxidative stressSignal TransductionToxicology
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Cholesterol burden in the liver induces mitochondrial dynamic changes and resistance to apoptosis

2018

Non-alcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of histopathological changes ranging from non-inflammatory intracellular fat deposition to non-alcoholic steatohepatitis (NASH), which may progress into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. Recent data suggest that impaired hepatic cholesterol homeostasis and its accumulation are relevant to the pathogenesis of NAFLD/NASH. Despite a vital physiological function of cholesterol, mitochondrial dysfunction is an important consequence of dietary-induced hypercholesterolemia and was, subsequently, linked to many pathophysiological conditions. The aim in the current study was to evaluate the morphological a…

Male0301 basic medicinemedicine.medical_specialtyTime FactorsCirrhosisPhysiologyClinical BiochemistryApoptosisMitochondria LiverMitochondrionDiet High-Fatmedicine.disease_causeMitochondrial DynamicsCholesterol Dietary03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsCells CulturedCell ProliferationCholesterolbusiness.industryFatty liverCell Biologymedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologyGene Expression RegulationLiverchemistry030220 oncology & carcinogenesisHepatocyteHepatocytesSteatohepatitisTranscriptomeHepatic fibrosisbusinessOxidative stressJournal of Cellular Physiology
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Sequential transcriptome analysis of human liver cancer indicates late stage acquisition of malignant traits

2014

Background & Aims Human hepatocarcinogenesis is as a multi-step process starting from dysplastic lesions to early carcinomas (eHCC) that ultimately progress to HCC (pHCC). However, the sequential molecular alterations driving malignant transformation of the pre-neoplastic lesions are not clearly defined. This lack of information represents a major challenge in the clinical management of patients at risk. Methods We applied next-generation transcriptome sequencing to tumor-free surrounding liver (n=7), low- (n=4) and high-grade (n=9) dysplastic lesions, eHCC (n=5) and pHCC (n=3) from 8 HCC patients with hepatitis B infection. Integrative analyses of genetic and transcriptomic changes were pe…

AdultMaleHepatocarcinogenesisCarcinoma HepatocellularCarcinogenesisBiologyBioinformaticsmedicine.disease_causePolymorphism Single NucleotideArticleMalignant transformationTranscriptomeCarcinomamedicineTumor MicroenvironmentHumansMolecular pathogenesisRNA NeoplasmGeneAgedTumor microenvironmentHepatologyGene Expression ProfilingLiver NeoplasmsWnt signaling pathwayRNA sequencingMiddle Agedmedicine.diseaseGene expression profilingCell Transformation NeoplasticMutationCancer researchDisease ProgressionFemaleCarcinogenesis
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