Lok Hei Chan
Associate Research Scientist in PathologyCards
About
Research
Publications
2025
LZTR1 is a melanoma oncogene that promotes invasion and suppresses apoptosis
Bacchiocchi A, Mak M, Khan Z, Gong X, Sznol M, Na Z, Su H, Chan L, Yan Q, Zhao D, Mortlock R, Knight J, Slavoff S, Halaban R. LZTR1 is a melanoma oncogene that promotes invasion and suppresses apoptosis. Oncogene 2025, 44: 3974-3984. PMID: 40885854, PMCID: PMC12500468, DOI: 10.1038/s41388-025-03538-2.Peer-Reviewed Original ResearchDegradation of ubiquitinated proteinsActin-related proteinsActin cytoskeleton organizationUbiquitin-proteasome systemSrc tyrosine kinaseAnchorage-independent growthNormal cell survivalCargo adapterActin organizationProximity biotinylationCytoskeleton organizationLC-MS/MS proteomicsLeucine zipperProteasome systemUbiquitinated proteinsCo-ImmunoprecipitationTargeting Pyk2Cell spreadingMelanoma cellsEnvironmental stressGrowth advantageMolecular characterizationCell migrationCell survivalLZTR1
2024
ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, PMCID: PMC11142404, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cells
2020
PRMT6 deficiency induces autophagy in hostile microenvironments of hepatocellular carcinoma tumors by regulating BAG5-associated HSC70 stability
Che N, Ng K, Wong T, Tong M, Kau P, Chan L, Lee T, Huen M, Yun J, Ma S. PRMT6 deficiency induces autophagy in hostile microenvironments of hepatocellular carcinoma tumors by regulating BAG5-associated HSC70 stability. Cancer Letters 2020, 501: 247-262. PMID: 33186656, DOI: 10.1016/j.canlet.2020.11.002.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsAutophagyCarcinoma, HepatocellularCell Line, TumorDrug Resistance, NeoplasmHep G2 CellsHSC70 Heat-Shock ProteinsHumansLiver NeoplasmsMaleMethylationMiceNeoplasm TransplantationNuclear ProteinsProtein StabilityProtein-Arginine N-MethyltransferasesReverse GeneticsSorafenibConceptsPost-translational methylationInversely correlated expressionCatalytic domainProtein arginine N-methyltransferase 6Cancer cellsHepatocellular carcinoma tumorsHostile microenvironmentAutophagy playersCellular biosynthesisGenetic approachesNutrient deprivationCellular homeostasisInduction of autophagyHepatocellular carcinoma cellsCritical survival factorBAG5Stressful microenvironmentCell survivalResponse to stressSurvival factorSensitivity to sorafenibStress conditionsAutophagyHepatocellular carcinomaHepatocellular carcinoma tissuesCRAF Methylation by PRMT6 Regulates Aerobic Glycolysis–Driven Hepatocarcinogenesis via ERK‐Dependent PKM2 Nuclear Relocalization and Activation
Wong T, Ng K, Tan K, Chan L, Zhou L, Che N, Hoo R, Lee T, Richard S, Lo C, Man K, Khong P, Ma S. CRAF Methylation by PRMT6 Regulates Aerobic Glycolysis–Driven Hepatocarcinogenesis via ERK‐Dependent PKM2 Nuclear Relocalization and Activation. Hepatology 2020, 71: 1279-1296. PMID: 31469916, DOI: 10.1002/hep.30923.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusCarcinogenesisCarcinoma, HepatocellularCell NucleusExtracellular Signal-Regulated MAP KinasesHep G2 CellsHumansLiver NeoplasmsMethylationNuclear ProteinsProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-rafPyruvate KinaseWarburg Effect, OncologicConceptsProtein arginine N-methyltransferase 6Human hepatocellular carcinomaTumor cellsSorafenib resistanceNuclear relocalizationTranscriptional repressor element 1-silencing transcription factorHuman hepatocellular carcinoma mouse modelAerobic glycolysisPyruvate kinase M2 isoformWarburg effectPatient-derived organoidsTarget of hypoxiaRepressor element-1 silencing transcription factorHepatocellular carcinomaDrug resistanceMouse modelAnimal modelsGlycolysis inhibitorGain-of-functionTherapeutic potentialM2 isoformSignaling AxisAnabolic growthGlucose metabolismTumorigenicity
2018
PRMT6 Regulates RAS/RAF Binding and MEK/ERK-Mediated Cancer Stemness Activities in Hepatocellular Carcinoma through CRAF Methylation
Chan L, Zhou L, Ng K, Wong T, Lee T, Sharma R, Loong J, Ching Y, Yuan Y, Xie D, Lo C, Man K, Artegiani B, Clevers H, Yan H, Leung S, Richard S, Guan X, Huen M, Ma S. PRMT6 Regulates RAS/RAF Binding and MEK/ERK-Mediated Cancer Stemness Activities in Hepatocellular Carcinoma through CRAF Methylation. Cell Reports 2018, 25: 690-701.e8. PMID: 30332648, DOI: 10.1016/j.celrep.2018.09.053.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCarcinoma, HepatocellularCell ProliferationDNA MethylationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMAP Kinase Kinase 1MAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, Inbred NODMice, KnockoutMice, NudeMice, SCIDNeoplastic Stem CellsNuclear ProteinsProtein-Arginine N-Methyltransferasesraf Kinasesras ProteinsTNF Receptor-Associated Factor 3Tumor Cells, CulturedXenograft Model Antitumor AssaysConceptsProtein-protein interaction studiesMEK/ERK signalingCell fate determinationPost-translational modificationsHepatocellular carcinomaRas bindingArginine methylationIntegrated transcriptomeRepressive functionFate determinationRas signalingHCC cell linesSignal transductionGene transcriptionAggressive cancer featuresCell linesRasLiver tumorigenesisHCC cellsHepatocellular carcinoma patientsCRAFPatient-derived organoidsGenesInteraction studiesArginine
2017
TP53INP1 Downregulation Activates a p73-Dependent DUSP10/ERK Signaling Pathway to Promote Metastasis of Hepatocellular Carcinoma
Ng K, Chan L, Chai S, Tong M, Guan X, Lee N, Yuan Y, Xie D, Lee T, Dusetti N, Carrier A, Ma S. TP53INP1 Downregulation Activates a p73-Dependent DUSP10/ERK Signaling Pathway to Promote Metastasis of Hepatocellular Carcinoma. Cancer Research 2017, 77: 4602-4612. PMID: 28674078, DOI: 10.1158/0008-5472.can-16-3456.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, HepatocellularCarrier ProteinsDual-Specificity PhosphatasesGene Expression ProfilingHeat-Shock ProteinsHumansLiver NeoplasmsLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase PhosphatasesNeoplasm MetastasisPrognosisProtein Array AnalysisSignal TransductionTumor Cells, CulturedTumor Protein p73Xenograft Model Antitumor AssaysConceptsHepatocellular carcinomaMetastatic progressionEarly-stage hepatocellular carcinomaAdvanced stage IVMetastatic hepatocellular carcinomaMetastatic progression of hepatocellular carcinomaMetastasis of hepatocellular carcinomaHuman HCC tumorsTP53INP1 downregulationProgression of hepatocellular carcinomaHCC tumorsP73-dependentStage IVTherapeutic strategiesTherapeutic opportunitiesERK pathwayHCC cellsCarcinomaMetastasisSignaling pathwayDownregulationTP53INP1DUSP10
2015
Turning Hepatic Cancer Stem Cells Inside Out – A Deeper Understanding through Multiple Perspectives
Chan L, Luk S, Ma S. Turning Hepatic Cancer Stem Cells Inside Out – A Deeper Understanding through Multiple Perspectives. Molecules And Cells 2015, 38: 202-209. PMID: 25666349, PMCID: PMC4363719, DOI: 10.14348/molcells.2015.2356.Peer-Reviewed Original ResearchConceptsCancer stem cellsHepatic cancer stem cellsHepatocellular carcinomaTumor cellsTumor microenvironmentRegulatory signaling networksPresence of cancer stem cellsStem cellsStem cell-like propertiesHeterogeneity of hepatocellular carcinomaLevel of tumorigenicitySignaling networksCell-like propertiesPutative originMalignancy of hepatocellular carcinomaEpigenetic alterationsSignaling pathwayTumor relapseDismal outcomeMalignant diseaseFrequent chemoresistanceCross-talkMetastatic abilityTumorTherapeutic strategies
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