Search results for "Cancer cell"

showing 10 items of 756 documents

Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
researchProduct

The Secreted Protein C10orf118 Is a New Regulator of Hyaluronan Synthesis Involved in Tumour-Stroma Cross-Talk.

2021

Simple Summary Hyaluronan is a main glycosaminoglycan in extracellular matrix with an important role in breast cancer progression. Alterations in its synthesis and size may affect tu-mour growth and metastasis. Communication between stromal and breast cancer cells consists of the secretion of factors that provoke a series of cell signalling that influence cell fate and tis-sue microenvironment, by favouring tumour cell survival and motility. Here, we present the c10orf118 protein expressed in high amounts by breast tumour cells as a new regulator in hya-luronan synthesis. This protein is found both in Golgi and secreted in the extracellular matrix, whereas its role is still unknown. The sec…

0301 basic medicineCancer ResearchChemokineBreast cancer; Estrogen receptor; Golgin104; Hyaluronan; Hyaluronan synthase 2; MCF-7; MDA-MB-231; Tumour microenvironmentMDA-MB-231Estrogen receptorBiologyHyaluronan Synthase 2lcsh:RC254-282ArticlehyaluronanGlycosaminoglycan03 medical and health scienceshyaluronan synthase 2breast cancer0302 clinical medicinemedicineSecretionCancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseCell biology030104 developmental biologyOncologyMCF-7030220 oncology & carcinogenesisCancer cellbiology.proteingolgin104MCF-7tumour microenvironmentestrogen receptorCancers
researchProduct

AKT3 Expression in Mesenchymal Colorectal Cancer Cells Drives Growth and Is Associated with Epithelial-Mesenchymal Transition

2021

Simple Summary Colorectal cancer can be subdivided into four distinct subtypes that are characterised by different clinical features and responses to therapies currently used in the clinic to treat this disease. One of those subtypes, called CMS4, is associated with a worse prognosis and poor response to therapies compared to other subtypes. We therefore set out to explore what proteins are differentially expressed and used in CMS4 to find potential new targets for therapy. We found that protein AKT3 is highly expressed in CMS4, and that active AKT3 inhibits a protein that stalls growth of cancer cells (p27KIP1). We can target AKT3 with inhibitors which leads to strongly reduced growth of c…

0301 basic medicineCancer ResearchColorectal cancergrowthBiologylcsh:RC254-282AKT3Article03 medical and health sciences0302 clinical medicinemedicinemesenchymal CRCEpithelial–mesenchymal transitionAKT3CMSMesenchymal stem cellCell cyclemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPhenotypeGene expression profiling030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioCancers
researchProduct

Effects of berberine, curcumin, resveratrol alone and in combination with chemotherapeutic drugs and signal transduction inhibitors on cancer cells-P…

2017

Over the past fifty years, society has become aware of the importance of a healthy diet in terms of human fitness and longevity. More recently, the concept of the beneficial effects of certain components of our diet and other compounds, that are consumed often by different cultures in various parts of the world, has become apparent. These “healthy” components of our diet are often referred to as nutraceuticals and they can prevent/suppress: aging, bacterial, fungal and viral infections, diabetes, inflammation, metabolic disorders and cardiovascular diseases and have other health-enhancing effects. Moreover, they are now often being investigated because of their anti-cancer properties/po…

0301 basic medicineCancer ResearchCurcuminBerberinemedia_common.quotation_subjectInflammationAntineoplastic AgentsPharmacologyResveratrol03 medical and health scienceschemistry.chemical_compoundNutraceuticalBerberineGeneticNeoplasmsGeneticsMedicineAnimalsHumansMolecular Biologymedia_commonbusiness.industryLongevityMetforminMetformin030104 developmental biologychemistryCardiovascular DiseasesResveratrolCancer cellDietary SupplementsCurcuminMolecular Medicinemedicine.symptombusinessBerberine; Curcumin; Metformin; Resveratrolmedicine.drugSignal TransductionAdvances in biological regulation
researchProduct

Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival.

2020

Abstract Metastatic melanoma is a fatal disease with a rapid systemic dissemination. The most frequent target sites are the liver, bone, and brain. Melanoma metastases represent a heterogeneous cell population, which associates with genomic instability and resistance to therapy. Interaction of melanoma cells with the hepatic sinusoidal endothelium initiates a signaling cascade involving cytokines, growth factors, bioactive lipids, and reactive oxygen and nitrogen species produced by the cancer cell, the endothelium, and also by different immune cells. Endothelial cell-derived NO and H2O2 and the action of immune cells cause the death of most melanoma cells that reach the hepatic microvascul…

0301 basic medicineCancer ResearchEndotheliumCell SurvivalPopulationCellmedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemDownregulation and upregulationTumor MicroenvironmentMedicineAnimalsHumansEndotheliumeducationMelanomaeducation.field_of_studybusiness.industryMelanomaLiver Neoplasmsmedicine.diseaseCarcinoma NeuroendocrineOxidative Stress030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellCancer researchbusinessOxidation-ReductionOxidative stressSeminars in cancer biology
researchProduct

A receptor-antibody hybrid hampering MET-driven metastatic spread

2021

AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…

0301 basic medicineCancer ResearchImmunoconjugatesmedicine.medical_treatmentMice SCIDEpitopeFusion proteins; HGF; MET; Metastasis; Targeted therapy; A549 Cells; Animals; Binding Sites Antibody; Cell Line Tumor; Cell Proliferation; Female; Hepatocyte Growth Factor; Humans; Immunoconjugates; Immunoglobulin Fab Fragments; Mice; Mice SCID; Neoplasm Metastasis; Neoplasms; Proto-Oncogene Proteins c-met; Rats; Rats Sprague-Dawley; Recombinant Proteins; Xenograft Model Antitumor AssaysMetastasisTargeted therapyMetastasisRats Sprague-DawleyTargeted therapyMice0302 clinical medicineNeoplasmsHGFNeoplasm MetastasisReceptorTumorHepatocyte Growth FactorChemistryProto-Oncogene Proteins c-metlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRecombinant ProteinsOncology030220 oncology & carcinogenesisMETFemaleHepatocyte growth factormedicine.drugSCIDlcsh:RC254-282Cell LineImmunoglobulin Fab Fragments03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansAntibodyCell ProliferationBinding SitesResearchmedicine.diseaseXenograft Model Antitumor AssaysFusion proteinRatsFusion proteins030104 developmental biologyA549 CellsCancer cellCancer researchBinding Sites AntibodySprague-DawleyJournal of Experimental & Clinical Cancer Research
researchProduct

Targeting the MET oncogene by concomitant inhibition of receptor and ligand via an antibody-"decoy" strategy

2018

MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and …

0301 basic medicineCancer ResearchLung NeoplasmsCellContext (language use)ApoptosisMice SCIDLigands03 medical and health sciencesMice0302 clinical medicineMice Inbred NODanti-HGF therapy; antibodies; decoy; MET oncogene; MET target therapyMET oncogeneExtracellularmedicineTumor Cells CulturedantibodiesAnimalsHumansdecoyCell ProliferationOncogenebiologyMET target therapyChemistryAntibodies MonoclonalProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysIn vitro030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer researchbiology.proteinanti-HGF therapyFemaleAntibodyDecoyGlioblastoma
researchProduct

LC3-Associated Phagocytosis (LAP): A Potentially Influential Mediator of Efferocytosis-Related Tumor Progression and Aggressiveness

2020

One aim of cancer therapies is to induce apoptosis of tumor cells. Efficient removal of the apoptotic cells requires coordinated efforts between the processes of efferocytosis and LC3-associated phagocytosis (LAP). However, this activity has also been shown to produce anti-inflammatory and immunosuppressive signals that can be utilized by live tumor cells to evade immune defense mechanisms, resulting in tumor progression and aggressiveness. In the absence of LAP, mice exhibit suppressed tumor growth during efferocytosis, while LAP-sufficient mice show enhanced tumor progression. Little is known about how LAP or its regulators directly affect efferocytosis, tumor growth and treatment respons…

0301 basic medicineCancer ResearchPhagocytosisReviewtumor cell apoptosislcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineCytotoxic T cellEfferocytosisefferocytosistumor immune responseTumor microenvironmentbusiness.industrydigestive oral and skin physiologyCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensM2 macrophage activation030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer cellLAPCancer researchbusinesshuman activitiesFrontiers in Oncology
researchProduct

Repurposing of plant alkaloids for cancer therapy: Pharmacology and toxicology.

2019

Drug repurposing (or repositioning) is an emerging concept to use old drugs for new treatment indications. Phytochemicals isolated from medicinal plants have been largely neglected in this context, although their pharmacological activities have been well investigated in the past, and they may have considerable potentials for repositioning. A grand number of plant alkaloids inhibit syngeneic or xenograft tumor growth in vivo. Molecular modes of action in cancer cells include induction of cell cycle arrest, intrinsic and extrinsic apoptosis, autophagy, inhibition of angiogenesis and glycolysis, stress and anti-inflammatory responses, regulation of immune functions, cellular differentiation, a…

0301 basic medicineCancer ResearchPhytochemicalsContext (language use)Antineoplastic AgentsPharmacologymedicine.disease_causeMetastasis03 medical and health sciences0302 clinical medicineAlkaloidsNeoplasmsDrug DiscoveryToxicity TestsmedicineAnimalsHumansRepurposingCardiotoxicitybusiness.industryDrug Repositioningmedicine.diseaseDrug repositioning030104 developmental biology030220 oncology & carcinogenesisCancer cellbusinessCarcinogenesisGenotoxicitySeminars in cancer biology
researchProduct

Betulinic acid induces a novel cell death pathway that depends on cardiolipin modification

2016

Cancer is associated with strong changes in lipid metabolism. For instance, normal cells take up fatty acids (FAs) from the circulation, while tumour cells generate their own and become dependent on de novo FA synthesis, which could provide a vulnerability to target tumour cells. Betulinic acid (BetA) is a natural compound that selectively kills tumour cells through an ill-defined mechanism that is independent of BAX and BAK, but depends on mitochondrial permeability transition-pore opening. Here we unravel this pathway and show that BetA inhibits the activity of steroyl-CoA-desaturase (SCD-1). This enzyme is overexpressed in tumour cells and critically important for cells that utilize de n…

0301 basic medicineCancer ResearchProgrammed cell deathCardiolipinsMitochondrionCell Line03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingBetulinic acidGeneticsCardiolipinHumansBetulinic AcidCytotoxicityMolecular BiologyCell DeathbiologyCytochrome cFatty AcidsCytochromes cLipid metabolismAntineoplastic Agents PhytogenicTriterpenesMitochondriaCell biology030104 developmental biologyBiochemistrychemistryCancer cellbiology.protein/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingPentacyclic TriterpenesStearoyl-CoA Desaturase
researchProduct