Search results for "HMGA"

showing 7 items of 7 documents

Unusual roles of caspase-8 in triple-negative breast cancer cell line MDA-MB-231

2015

Triple-negative breast cancer (TNBC) is a clinically aggressive form of breast cancer that is unresponsive to endocrine agents or trastuzumab. TNBC accounts for ~10-20% of all breast cancer cases and represents the form with the poorest prognosis. Patients with TNBC are at higher risk of early recurrence, mainly in the lungs, brain and soft tissue, therefore, there is an urgent need for new therapies. The present study was carried out in MDA-MB-231 cells, where we assessed the role of caspase-8 (casp-8), a critical effector of death receptors, also involved in non‑apoptotic functions. Analysis of casp-8 mRNA and protein levels indicated that they were up-regulated with respect to the normal…

0301 basic medicineMDA-MB-231 cellCancer ResearchDown-RegulationTriple Negative Breast NeoplasmsTransfectionResting Phase Cell Cycle03 medical and health sciencesKruppel-Like Factor 40302 clinical medicineHMGA2Breast cancerCell Line TumormedicineHumansRNA Small InterferingCaspase-8 unusual roleTriple-negative breast cancerCaspase 8Triple-negative breast cancer cellbiologyOncogeneCaspase-8 knockdownCell CycleG1 PhaseCancerCell cyclemedicine.diseaseMolecular medicineKLF4Invasivity and metastasi030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleCell cycle regulator
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12q14.3 microdeletion involving HMGA2 gene cause a Silver-Russell syndrome-like phenotype: a case report and review of the literature

2020

Abstract Background Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction and normal head circumference with consequent relative macrocephaly. Addictional findings are protruding forehead in early life, body asymmetry (of upper and lower limbs) and substantial feeding difficulties. Although several genetic mechanisms that cause the syndrome are known, more than 40% of patients with a SRS-like phenotype remain without an etiological diagnosis. In the last few years, different clinical reports have suggested that mutations or deletions of the HMGA2 gene can be responsible for a SRS-like phenotype in patients with negative results of…

0301 basic medicineMaleCase Report030105 genetics & heredityBioinformaticsHMGA2 gene03 medical and health sciencesHMGA2parasitic diseasesmedicineHumansGeneChromosome 12biologybusiness.industrySilver–Russell syndromeNetchine-Harbison clinical scoring systemHMGA2 Proteinlcsh:RJ1-570Genetic disorderlcsh:PediatricsFailure to thrivemedicine.diseasePhenotypeSilver-Russell Syndrome030104 developmental biologyPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolFailure to thriveEtiologybiology.proteinmedicine.symptombusinessGene DeletionItalian Journal of Pediatrics
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Overexpression of the truncated form of high mobility group a proteins (HMGA2) in human myometrial cells induces leiomyoma-like tissue formation

2014

The pathogenesis of uterine leiomyomas, the most common benign tumor in women, is still unknown. This lack of basic knowledge limits the development of novel non-invasive therapies. Our group has previously demonstrated that leiomyoma side population (SP) cells are present in tumor lesions and act like putative tumor-initiating stemcells in human leiomyoma. Moreover, accumulated evidence demonstrates that these benign tumors of mesenchymal origin are characterized by rearrangements of the High Mobility Group A proteins (HMGA). In this work, we tested the hypothesis that leiomyoma development may be due to overexpression of HMGA2 (encoding high mobility group AT-hook2) in myometrial stem cel…

EmbryologyMice SCID//purl.org/becyt/ford/1 [https]MiceMice Inbred NODProtein IsoformsUterine leiomyomaLeiomyomaStem CellsSOMATIC STEM CELLSObstetrics and GynecologyExonsBioquímica y Biología Molecularfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticCell Transformation NeoplasticLeiomyomaUterine NeoplasmsMyometriumNeoplastic Stem CellsFemaleStem cellHIGH MOBILITY GROUP A PROTEINSCIENCIAS NATURALES Y EXACTASPlasmidsAdult stem cellmedicine.medical_specialtyUTERINE LEIOMYOMASMyocytes Smooth MuscleTransplantation HeterologousBiologyTransfectionHUMAN MYOMETRIUMCiencias BiológicasHMGA2Side populationInternal medicineGeneticsmedicineAnimalsHumans//purl.org/becyt/ford/1.6 [https]neoplasmsMolecular BiologyHMGA2 ProteinMesenchymal stem cellHMGASIDE POPULATIONCell Biologymedicine.diseaseIntronsEndocrinologyReproductive MedicineCancer researchbiology.proteinDevelopmental Biology
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The HMGA1 protoncogene frequently deregulated in cancer is a transcriptional target of E2F1

2011

Reactivation of the HMGA1 protoncogene is very frequent in human cancer, but still very little is known on the molecular mechanisms leading to this event. Prompted by the finding of putative E2F binding sites in the human HMGA1 promoter and by the frequent deregulation of the RB/E2F1 pathway in human carcinogenesis, we investigated whether E2F1 might contribute to the regulation of HMGA1 gene expression. Here we report that E2F1 induces HMGA1 by interacting with a 193bp region of the HMGA1 promoter containing an E2F binding site surrounded by three putative Sp1 binding sites. Both gain and loss of function experiments indicate that Sp1 functionally interacts with E2F1 to promote HMGA1 expre…

Transcriptional ActivationChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternMolecular Sequence DataReal-Time Polymerase Chain ReactionRetinoblastoma ProteinSp1MiceAnimalsHumansPituitary NeoplasmsThyroid NeoplasmsHMGA1a ProteinPituitary NeoplasmRNA MessengerPromoter Regions GeneticCarcinogenesiThyroid NeoplasmHMGA1 promoterMice KnockoutBinding SitesBase SequenceAnimalReverse Transcriptase Polymerase Chain ReactionBinding SiteMutationMutagenesis Site-DirectedTranscriptionE2F1 Transcription FactorHumansp1; carcinogenesis; hmga1 promoter; transcription
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Human Papilloma Virus-Dependent HMGA1 Expression Is a Relevant Step in Cervical Carcinogenesis

2008

HMGA1 is a member of a small family of architectural transcription factors involved in the coordinate assembly of multiprotein complexes referred to as enhanceosomes. In addition to their role in cell proliferation, differentiation, and development, high-mobility group proteins of the A type (HMGA) family members behave as transforming protoncogenes either in vitro or in animal models. Recent reports indicated that HMGA1 might counteract p53 pathway and provided an interesting hint on the mechanisms determining HMGA's transforming potential. HMGA1 expression is deregulated in a very large array of human tumors, including cervical cancer, but very limited information is available on the mole…

Uterine Cervical NeoplasmCancer ResearchDNA-Binding ProteinBiologyHeLa Celllcsh:RC254-282DNA-binding proteinRNA interferenceCell Line TumorHMGA1a ProteinRNA MessengerReceptor Notch1PapillomaviridaePapillomavirus InfectionPsychological repressionTranscription factorCell ProliferationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingHMGAOncogene Proteins ViralCell Transformation Virallcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA1Gene Expression Regulation NeoplasticGene expression profilingCancer cellCancer researchbiology.proteinFemaleTumor Suppressor Protein p53HumanNeoplasia
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Genetic and Molecular Characterization of The Human Osteosarcoma 3AB-OS Cancer Stem Cell Line: A Possible Model For Studying Osteosarcoma Origin and …

2013

Finding new treatments targeting cancer stem cells (CSCs) within a tumor seems to be critical to halt cancer and improve patient survival. Osteosarcoma is an aggressive tumor affecting adolescents, for which there is no second-line chemotherapy. Uncovering new molecular mechanisms underlying the development of osteosarcoma and origin of CSCs is crucial to identify new possible therapeutic strategies. Here, we aimed to characterize genetically and molecularly the human osteosarcoma 3AB-OS CSC line, previously selected from MG63 cells and which proved to have both in vitro and in vivo features of CSCs. Classic cytogenetic studies demonstrated that 3AB-OS cells have hypertriploid karyotype wit…

cancer stem cellsPhysiologyClinical Biochemistrymedicine.disease_causePolymerase Chain ReactionOsteosarcoma cancer stem cellSettore BIO/10 - BiochimicaChromosomes HumanGene Regulatory NetworksCopy-number variationOligonucleotide Array Sequence AnalysisGeneticsComparative Genomic HybridizationOsteosarcomabiologychromosomal aberrationGene Expression Regulation NeoplasticPhenotypemiRNAsNeoplastic Stem CellsOsteosarcomaMitosisBone NeoplasmsHMGA2Cancer stem cellCell Line TumormicroRNABiomarkers Tumorgene expression profilingmedicineHumansOsteosarcoma cancer stem cells; karyotype; chromosomal aberrations; gene expression profiling; miRNAsCell LineageGenetic Predisposition to DiseaseRNA MessengerCell NucleusChromosome AberrationsPloidiesModels GeneticComputational BiologyCancerCell Biologymedicine.diseasekaryotypeMicroRNAsKaryotypingbiology.proteinCancer researchCarcinogenesisComparative genomic hybridization
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Molecular mechanisms of MYCN-dependent apoptosis and the MDM2-p53 pathway: an Achille’s heel to be exploited for the therapy of MYCN amplified neurob…

2012

The p53 oncosuppressor is very seldom mutated in neuroblastoma, but several mecha- nisms cooperate to its functional inactivation in this tumor. Increased MDM2 levels, due to genetic amplification or constitutive inhibition of p14ARF, significantly contribute to this event highlighting p53 reactivation as an attractive perspective for neuroblastoma treat- ment. In addition to its role in tumorigenesis, MYCN sensitizes untransformed and cancer cells to apoptosis. This is associated to a fine modulation of the MDM2-p53 pathway Indeed MYCN induces p53 and MDM2 transcription, and, by evoking a DNA damage response (DDR), it stabilizes p53 and its proapoptotic kinase Homeodomain Interacting Prote…

p53Programmed cell deathCancer ResearchHMGA1HIPK2Biologymedicine.disease_causelcsh:RC254-28203 medical and health sciencesNeuroblastoma0302 clinical medicineMDM2NeuroblastomaMYCNmedicineProtein kinase Aneoplasms030304 developmental biology0303 health sciencesKinaseHMGA1amedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA13. Good healthOncology030220 oncology & carcinogenesisCancer cellPerspective ArticleMDM2-antagonistsbiology.proteinCancer researchMdm2CarcinogenesisMDM2-antagonistFrontiers in Oncology
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