2022
N-nitrosamines-mediated downregulation of LncRNA-UCA1 induces carcinogenesis of esophageal squamous by regulating the alternative splicing of FGFR2
Wang X, Sun M, Gao Z, Yin L, Pu Y, Zhu Y, Wang X, Liu R. N-nitrosamines-mediated downregulation of LncRNA-UCA1 induces carcinogenesis of esophageal squamous by regulating the alternative splicing of FGFR2. The Science Of The Total Environment 2022, 855: 158918. PMID: 36169023, DOI: 10.1016/j.scitotenv.2022.158918.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingCarcinogenesisCell Line, TumorCell MovementCell ProliferationDown-RegulationEpigenesis, GeneticEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansMicroRNAsNitrosaminesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 2RNA, Long NoncodingConceptsFibroblast growth factor receptor 2Alternative splicingEsophageal squamous cell carcinomaExact molecular mechanismsHet-1A cellsDownregulation of UCA1Epithelial-mesenchymal transitionPI3K-AKT axisFGFR2-IIIcMolecular mechanismsPI3K-AktF proteinUnknown mechanismESCC cellsESCC progressionSplicingN-nitrosamine exposureGrowth factor receptor 2Squamous cell carcinomaDigestive system tumorsRegulation levelESCC tissuesFactor receptor 2High incidence areaLncRNA UCA1
2009
Cancer-related transcriptional targets of the circadian gene NPAS2 identified by genome-wide ChIP-on-chip analysis
Yi CH, Zheng T, Leaderer D, Hoffman A, Zhu Y. Cancer-related transcriptional targets of the circadian gene NPAS2 identified by genome-wide ChIP-on-chip analysis. Cancer Letters 2009, 284: 149-156. PMID: 19457610, PMCID: PMC3182267, DOI: 10.1016/j.canlet.2009.04.017.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaBasic Helix-Loop-Helix Transcription FactorsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticChromatin ImmunoprecipitationCircadian RhythmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksGenome-Wide Association StudyHumansNeoplasm ProteinsNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisRNA InterferenceRNA, Small InterferingTranscription, GeneticConceptsDirect transcriptional targetTranscriptional targetsCircadian genesGenome-wide mapping approachChip analysisGenome-wide ChIPCancer-related gene expressionCore circadian genesRelevant biological pathwaysTranscriptional profilesGene expressionReal-time PCR assaysBiological processesCell cycleBiological pathwaysNPAS2Biological involvementGenesHuman cancersMCF-7 cellsCancer developmentTumorigenesisPCR assaysCircadian rhythmTarget
2004
Methyl‐CpG‐binding domain 2
Zhu Y, Spitz M, Zhang H, Grossman H, Frazier M, Wu X. Methyl‐CpG‐binding domain 2. Cancer 2004, 100: 1853-1858. PMID: 15112265, DOI: 10.1002/cncr.20199.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceCase-Control StudiesDNA MethylationDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansLogistic ModelsMaleMolecular Sequence DataOdds RatioProbabilityPrognosisPromoter Regions, GeneticReference ValuesReverse Transcriptase Polymerase Chain ReactionRisk FactorsRNA, MessengerSensitivity and SpecificityUrinary Bladder NeoplasmsConceptsMBD2 expressionCarcinoma riskCurrent case-control studyReverse transcription polymerase chain reaction assaysCase-control studyPeripheral blood lymphocytesQuantitative reverse transcription-polymerase chain reaction assaysTranscription-polymerase chain reaction assaysMessenger RNA expressionReal-time quantitative reverse transcription-polymerase chain reaction assaysControl patientsLight smokersCase patientsHeavy smokersUnderlying molecular mechanismsTumor tissue typesBlood lymphocytesChain reaction assaysProtective effectProtective roleQuartile distributionDomain 2 proteinOlder individualsTumor developmentYoung individuals