Search results for " Sen"

showing 10 items of 5232 documents

Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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The role of surgery in platinum-resistant ovarian cancer: A call to the scientific community.

2021

Abstract In the last decade, a growing attention has been focused on identifying effective therapeutic strategies also in the orphan clinical setting of women with platinum-resistant disease. In this context, secondary cytoreductive surgery (SCS) remains a potential approach only in women with platinum sensitive relapse, but experimental data have been published supporting the role of SCS also in patients with platinum-resistant recurrence. In particular, surgery is emerging as a potential option in specific subgroups of women, such as those patients with low-grade serous histology, or low-volume relapse with disease located in the so-called pharmacological sanctuaries. Furthermore, contras…

0301 basic medicineCancer Researchmedicine.medical_specialtymedicine.medical_treatmentContext (language use)Antineoplastic AgentsPlatinum CompoundsDiseaseHyperthermic Intraperitoneal ChemotherapyCarcinoma Ovarian Epithelial03 medical and health sciences0302 clinical medicineMedicineAnimalsHumansIn patientPlatinum resistantChemotherapybusiness.industryCytoreduction Surgical Proceduresmedicine.diseaseCombined Modality TherapySurgerySerous fluid030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisPlatinum sensitiveFemaleNeoplasm Recurrence LocalbusinessOvarian cancerBiological features Minimally invasive surgery Personalized treatment Platinum resistant Recurrent ovarian cancer Secondary cytoreductive surgerySeminars in cancer biology
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Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
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Physiological concentrations of phytosterols enhance the apoptotic effects of 5-fluorouracil in colon cancer cells

2018

Abstract Combining natural products as co-adjuvants in 5-fluorouracil (5-FU) chemotherapy might enhance the effectiveness of 5-FU by avoiding a high dosage and/or reducing treatment times. We explored the anticancer efficacy of the phytosterols (PS) at concentrations achievable in the human colon, as well as their potential as sensitizing agents of human colon cancer cells (Caco-2 and HT-29) to 5-FU treatment. Cells proliferation, combination index, cell cycle, apoptosis, caspases activation, ROS production, and ΔΨm were determined. Co-treatment (PS+5-FU) had an antiproliferative additive effect, and moreover, in general a significantly improved efficacy was observed on cell cycle arrest at…

0301 basic medicineCell cycle checkpointColorectal cancermedicine.medical_treatmentMedicine (miscellaneous)ApoptosisCell cycle03 medical and health sciences0302 clinical medicineIn vivomedicine5-fluorouracilTX341-641Colon cancer cellsCaspaseChemotherapyNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryPhytosterolsCell cyclemedicine.disease030104 developmental biologyApoptosisFluorouracil030220 oncology & carcinogenesisCancer researchbiology.proteinDrug sensitivityFood Sciencemedicine.drugJournal of Functional Foods
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Signalling strength determines proapoptotic functions of STING

2017

Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prev…

0301 basic medicineCell typeLeukemia T-CellTranscription Geneticmedicine.medical_treatmentScienceCellsT-LymphocytesGeneral Physics and AstronomyActivationApoptosisInnate Immune SensorBiologyCytosolic DnaCgasGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCyclic Gmp-Amp[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineAnimalsReceptorlcsh:ScienceMultidisciplinaryInnate immune systemEffectorQ2nd-MessengerMembrane ProteinsGeneral ChemistryHedgehog signaling pathwayeye diseases3. Good healthCell biologyMice Inbred C57BLSting030104 developmental biologyCytokineDi-GmpImmunologylcsh:QInterferon Regulatory Factor-3Signal transductionTumor Suppressor Protein p53InfectionProtein BindingSignal TransductionNature Communications
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Analysis of RNA modifications by liquid chromatography–tandem mass spectrometry

2016

The analysis of RNA modifications is of high importance in order to address a wide range of biological questions. Therefore, a highly sensitive and accurate method such as liquid chromatography-tandem mass spectrometry (LC-MS/MS) has to be available. By using different LC-MS/MS procedures, it is not only possible to quantify very low amounts of RNA modifications, but also to detect probably unknown modified nucleosides. For these cases the dynamic multiple reaction monitoring and the neutral loss scan are the most common techniques. Here, we provide the whole workflow for analyzing RNA samples regarding their modification content. This includes an equipment list, the preparation of required…

0301 basic medicineChromatographyChemistrySelected reaction monitoringMs analysisRNATandem mass spectrometryMass spectrometryModified nucleosidesGeneral Biochemistry Genetics and Molecular BiologyHighly sensitive03 medical and health sciences030104 developmental biologyTandem Mass SpectrometryLiquid chromatography–mass spectrometryHumansRNARNA Processing Post-TranscriptionalMolecular BiologyChromatography LiquidMethods
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Collective behavior of quorum-sensing run-and-tumble particles in confinement

2016

We study a generic model for quorum-sensing bacteria in circular confinement. Every bacterium produces signaling molecules, the local concentration of which triggers a response when a certain threshold is reached. If this response lowers the motility then an aggregation of bacteria occurs, which differs fundamentally from standard motility-induced phase separation due to the long-ranged nature of the concentration of signal molecules. We analyze this phenomenon analytically and by numerical simulations employing two different protocols leading to stationary cluster and ring morphologies, respectively.

0301 basic medicineCollective behaviorGeneral Physics and AstronomyFOS: Physical sciencesNanotechnologyCondensed Matter - Soft Condensed MatterBacterial Physiological Phenomena01 natural sciencesSignalModels BiologicalQuantitative Biology::Cell BehaviorQuantitative Biology::Subcellular Processes03 medical and health sciences0103 physical sciencesCell Behavior (q-bio.CB)Cluster (physics)Physics - Biological Physics010306 general physicsCondensed Matter - Statistical MechanicsPhysicsStatistical Mechanics (cond-mat.stat-mech)ChemotaxisQuorum SensingQuorum sensing030104 developmental biologyChemical physicsBiological Physics (physics.bio-ph)FOS: Biological sciencesQuantitative Biology - Cell BehaviorSoft Condensed Matter (cond-mat.soft)
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