0000000000287800

AUTHOR

Tobias Schilling

showing 5 related works from this author

Chemotherapy-induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediatedviathe extrinsic and the intrinsic pathway

2010

We investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95-, the TNF- and the TRAIL-receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each o…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor geneDNA damagetumor suppressor protein p53membrane proteinsoligonucleotide array sequence analysiscarcinomaBiologyhepatocellularfas-associated death domain proteinAPAF1humansMembrane Potential Mitochondrialhep G2 cellsbleomycinliver neoplasmsSettore BIO/11apoptosisPrognosismitochondrialFas receptorcaspasesOncologyApoptosisbiology.proteinCancer researchMdm2membrane potentialSignal transductionPrognosis; bleomycin; caspases; membrane potential mitochondrial; oligonucleotide array sequence analysis; tumor suppressor protein p53; membrane proteins; fas-associated death domain protein; humans; liver neoplasms; hep G2 cells; apoptosis; carcinoma hepatocellularInternational Journal of Cancer
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Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma.

2006

AbstractInhibition of cyclooxygenase (COX)-2 elicits chemopreventive and therapeutic effects in solid tumors that are coupled with the induction of apoptosis in tumor cells. We investigated the mechanisms by which COX-2 inhibition induces apoptosis in hepatocellular carcinoma (HCC) cells. COX-2 inhibition triggered expression of the CD95, tumor necrosis factor (TNF)-R, and TNF-related apoptosis-inducing ligand (TRAIL)-R1 and TRAIL-R2 death receptors. Addition of the respective specific ligands further increased apoptosis, indicating that COX-2 inhibition induced the expression of functional death receptors. Overexpression of a dominant-negative Fas-associated death domain mutant reduced COX…

Cancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma HepatocellularApoptosisMitochondria LiverBiologyTransfectionReceptors Tumor Necrosis FactorInternal medicineCell Line TumormedicineHumansfas ReceptorDeath domainInhibitor of apoptosis domainSulfonamidesCyclooxygenase 2 InhibitorsIntrinsic apoptosisLiver NeoplasmsFas receptorReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyOncologyUVB-induced apoptosisApoptosisCelecoxibCyclooxygenase 2Cancer researchPyrazolesSignal transductionSignal TransductionCancer research
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Regulation of PTHrP and PTH/PTHrP receptor by extracellular Ca2+ concentration and hormones in the breast cancer cell line 8701-BC.

2000

AbstractIt was previously reported that 8701-BC breast tumour cells express the gene for parathyroid hormonerelated peptide (PTHrP) and PTH/PTHrP receptor (PTHrPR) and release immunoreactive PTHrP (iPTHrP) into the extracellular medium. Since the regulation of PTHrP and PTHrPR by breast cancer cells has been poorly investigated so far, we have chosen the 8701- BC cell line as a model system to investigate whether alterations in the extracellular Ca[2+] concentration ([Ca[2+]]) and treatment with some wellknown differentiation agents for breast cells, such as dimethyl sulfoxide, hydrocortisone, progesterone, prolactin, alltrans retinoic acid and transforming growth factorβ1 might (i) modulat…

medicine.medical_specialtyTranscription GeneticRNA SplicingClinical BiochemistryRetinoic acidCodon InitiatorBreast NeoplasmsTretinoinBiochemistrychemistry.chemical_compoundTranscription (biology)Transforming Growth Factor betaInternal medicinemedicineExtracellularTumor Cells CulturedHumansProtein IsoformsRNA MessengerPromoter Regions GeneticMolecular BiologyGeneChemistryParathyroid Hormone-Related ProteinProteinsProlactinHormonesNeoplasm ProteinsEndocrinologyGene Expression RegulationCell cultureRNA splicingReceptors Parathyroid HormoneCalciumExtracellular Spacehormones hormone substitutes and hormone antagonistsHormoneBiological chemistry
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ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

2010

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.ΔNp73β can directly interfere with the transcriptional activation function of the TA (containing the t…

Gene isoformCarcinoma HepatocellularMolecular Sequence DataApoptosisBiologyModels BiologicalTransactivationDownregulation and upregulationCell Line TumorHumansProtein IsoformsMolecular BiologyTranscription factorGenes DominantOligonucleotide Array Sequence Analysisbcl-2-Associated X ProteinRegulation of gene expressionBase SequenceSettore BIO/11Gene Expression ProfilingTumor Suppressor ProteinsLiver NeoplasmsNuclear ProteinsTumor Protein p73PromoterReceptors Death DomainCell BiologyCell cyclePrognosisMitochondriaCell biologyDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation NeoplasticDrug Resistance NeoplasmCaspasesCancer researchTumor Suppressor Protein p53Signal transductionPrecancerous ConditionsSignal TransductionDevelopmental BiologyCell Cycle
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Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

1999

AbstractIt was previously reported that 8701-BC breast cancer cells express the gene for parathyroid hormone-related peptide (PTHrP) and its cognate receptor (PTHrP-R), and release immunoreactive PTHrP in the extracellular medium; it was also found that PTHrP, in turn, exerts a role on the proliferative and invasive behavior in vitro of the same cell line. On the other hand, evidence has been produced that adhesion of 8701-BC cells onto different collagen substrates influences in various ways a number of phenotypic expressions, such as cell growth, motility, invasion of reconstituted basement membrane and production of lytic enzymes of the extracellular matrix (ECM). In light of these previ…

musculoskeletal diseasesmedicine.medical_specialtyParathyroid hormone-related peptideStromal cellRNA SplicingCellular differentiationBiophysicsBreast NeoplasmsBiologyPolymerase Chain ReactionBiochemistryExtracellular matrixBreast cancerStructural BiologyLamininInternal medicineGene expressionTumor Cells CulturedGeneticsmedicineExtracellularHumansParathyroid hormone-related peptide receptorMolecular BiologyReceptor Parathyroid Hormone Type 1Basement membraneParathyroid Hormone-Related ProteinProteinsCell DifferentiationCell Biologymusculoskeletal systemExtracellular MatrixNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticDrug CombinationsEndocrinologymedicine.anatomical_structureCell culturebiology.proteinReceptors Parathyroid HormoneProteoglycansGene expressionCollagenLamininhormones hormone substitutes and hormone antagonistsFEBS Letters
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