Search results for "Oncology"

showing 10 items of 10554 documents

VEGF-R2/Caveolin-1 Pathway of Undifferentiated ARPE-19 Retina Cells: A Potential Target as Anti-VEGF-A Therapy in Wet AMD by Resvega, an Omega-3/Poly…

2021

Age-related macular degeneration (AMD) is one of the main causes of deterioration in vision in adults aged 55 and older. In spite of therapies, the progression of the disease is often observed without reverse vision quality. In the present study, we explored whether, in undifferentiated ARPE-19 retinal cells, a disruption of the VEGF receptors (VEGF-R)/caveolin-1 (Cav-1)/protein kinases pathway could be a target for counteracting VEGF secretion. We highlight that Resvega®, a combination of omega-3 fatty acids with an antioxidant, resveratrol, inhibits VEGF-A secretion in vitro by disrupting the dissociation of the VEGF-R2/Cav-1 complex into rafts and subsequently preventing MAPK activation.…

0301 basic medicineMAP Kinase Signaling SystemAngiogenesisQH301-705.5Caveolin 1Drug Evaluation PreclinicalresveratrolResveratrolAMDRetinaArticleCatalysisCell LineVEGF-receptorInorganic ChemistryMacular Degeneration03 medical and health scienceschemistry.chemical_compoundangiogenesis0302 clinical medicinemedicineHumansSecretionPhysical and Theoretical ChemistryBiology (General)Molecular BiologyQD1-999SpectroscopyRetinaomega-3 fatty acidsKinaseOrganic Chemistryocular diseasesRetinalGeneral MedicineVascular Endothelial Growth Factor Receptor-2VEGFIn vitroComputer Science ApplicationsTranscription Factor AP-1Chemistry030104 developmental biologymedicine.anatomical_structurechemistry030220 oncology & carcinogenesisCaveolin 1Cancer researchInternational Journal of Molecular Sciences
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Integrated analysis of colorectal cancer microRNA datasets: Identification of microRNAs associated with tumor development

2018

Colorectal cancer (CRC) is one of the leading cause of cancer death worldwide. Currently, no effective early diagnostic biomarkers are available for colorectal carcinoma. Therefore, there is a need to discover new molecules able to identify pre-cancerous lesions. Recently, microRNAs (miRNAs) have been associated with the onset of specific pathologies, thus the identification of miRNAs associated to colorectal cancer may be used to detect this pathology at early stages. On these bases, the expression levels of miRNAs were analyzed to compare the miRNAs expression levels of colorectal cancer samples and normal tissues in several miRNA datasets. This analysis revealed a group of 19 differentia…

0301 basic medicineMAPK/ERK pathwayAgingColorectal cancerDatasets as TopicBiology03 medical and health sciences0302 clinical medicineMismatch Repair PathwaymicroRNAmedicineHumansSettore MED/05 - Patologia ClinicaGenePI3K/AKT/mTOR pathwayBioinformaticWnt signaling pathwayMicroRNAbioinformaticsBiomarkerCell Biologymedicine.diseaseColorectal cancerBiomarker (cell)MicroRNAs030104 developmental biology030220 oncology & carcinogenesisBioinformatics; Biomarker; Colorectal cancer; Dataset; MicroRNA; Aging; Cell BiologyCancer researchColorectal NeoplasmsTranscriptomeResearch PaperDataset
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Targeting BRAF and RAS in Colorectal Cancer

2021

Simple Summary In colorectal cancer, mutations of the KRAS and BRAF genes are quite common and can contribute to the activation of cell signaling pathways that lead to cell proliferation and differentiation. These processes promote cancer growth, and in some cases, they may cause cells to develop resistance to certain types of treatment, notably EGFR inhibitors. We summarize recent knowledge regarding the effects of KRAS and BRAF mutations in the setting of colorectal cancer and discuss the new therapies under development. Abstract Colorectal cancer (CRC) is still one of the most frequent forms of cancer in the world in terms of incidence. Around 40% of CRC patients carry a mutation of the …

0301 basic medicineMAPK/ERK pathwayCancer ResearchColorectal cancerAngiogenesismedicine.medical_treatmentcolorectal cancerReviewmedicine.disease_causeBRAFTargeted therapy03 medical and health sciences0302 clinical medicineKRASmedicineneoplasmsRC254-282EGFR inhibitorsMutationbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensCancertargeted therapymedicine.diseasedigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchKRASbusinessCancers
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Therapeutic resistance in breast cancer cells can result from deregulated EGFR signaling

2020

The epidermal growth factor receptor (EGFR) interacts with various downstream molecules including phospholipase C (PLC)/protein kinase C (PKC), Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/GSK-3, Jak/STAT and others. Often these pathways are deregulated in human malignancies such as breast cancer. Various therapeutic approaches to inhibit the activity of EGFR family members including small molecule inhibitors and monoclonal antibodies (MoAb) have been developed. A common problem with cancer treatments is the development of drug-resistance. We examined the effects of a conditionally-activated EGFR (v-Erb-B:ER) on the resistance of breast cancer cells to commonly used chemotherapeutic drugs such as doxorub…

0301 basic medicineMAPK/ERK pathwayEGFRvIIICancer ResearchEGFREstrogen receptorAntineoplastic AgentsBreast Neoplasms03 medical and health sciences0302 clinical medicineBreast cancerBreast cancerCell Line TumorGeneticsHumansMedicinePTENEpidermal growth factor receptorskin and connective tissue diseasesMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologybusiness.industryCancermedicine.diseaseErbB Receptors030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDrug resistancebiology.proteinCancer researchMolecular MedicineFemalebusinessSignal TransductionV-Erb-B
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Mycobacterium tuberculosis Rv2145c Promotes Intracellular Survival by STAT3 and IL-10 Receptor Signaling

2021

Although Mycobacterium tuberculosis (Mtb) is an intracellular pathogen in phagocytic cells, the factors and mechanisms by which they invade and persist in host cells are still not well understood. Characterization of the bacterial proteins modulating macrophage function is essential for understanding tuberculosis pathogenesis and bacterial virulence. Here we investigated the pathogenic role of the Rv2145c protein in stimulating IL-10 production. We first found that recombinant Rv2145c stimulated bone marrow-derived macrophages (BMDMs) to secrete IL-10, IL-6 and TNF-α but not IL-12p70 and to increase the expression of surface molecules through the MAPK, NF-κB, and TLR4 pathways and enhanced …

0301 basic medicineMAPK/ERK pathwayImmunologyMicrobiologySTAT3Mycobacterium tuberculosis03 medical and health sciencesRv2145c0302 clinical medicineImmunology and AllergyMacrophageSecretionOriginal Researchpathogenic rolebiologyMycobacterium smegmatisMycobacterium tuberculosisRC581-607biology.organism_classificationInterleukin 10030104 developmental biology030220 oncology & carcinogenesisIL-10TLR4Immunologic diseases. AllergyIntracellularFrontiers in Immunology
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Modulation of the TGF-β1-induced epithelial to mesenchymal transition (EMT) mediated by P1 and P2 purine receptors in MDCK cells

2017

Epithelial to mesenchymal transition (EMT) occurs during embryogenesis or under pathological conditions such as hypoxia, injury, chronic inflammation, or tissue fibrosis. In renal tubular epithelial cells (MDCK), TGF-β1 induces EMT by reducing or increasing epithelial or mesenchymal marker expression, respectively. In this study, we confirmed that the cAMP analogues, 8-CPT-cAMP or N6-Ph-cAMP, inhibited the TGF-β1-driven overexpression of the mesenchymal markers ZEB-1, Slug, Fibronectin, and α-SMA. Furthermore, we showed that A1, A2A, P2Y1, P2Y11, and P2X7 purine receptor agonists modulated the TGF-β1-induced EMT through the involvement of PKA and/or MAPK/ERK signaling. The stimulation o…

0301 basic medicineMAPK/ERK pathwayMadin Darby canine kidney cellEpithelial-Mesenchymal TransitionFibrosiCellTransforming growth factor β1InflammationStimulationBiologyEpithelial to mesenchymal transition; Fibrosis; Madin Darby canine kidney cells; P1/P2 purinergic receptors; Transforming growth factor β1; Molecular Biology; Cellular and Molecular Neuroscience; Cell BiologyTransforming Growth Factor beta103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDogsmedicineAnimalsEpithelial–mesenchymal transitionReceptorMolecular BiologyEpithelial to mesenchymal transitionP1/P2 purinergic receptorReceptors Purinergic P2Mesenchymal stem cellReceptors Purinergic P1Cell BiologyMadin Darby canine kidney cellsFibrosisCell biologyFibronectin030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinP1/P2 purinergic receptorsOriginal ArticleTransforming growth factor β1medicine.symptomTransforming growth factor
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ERK3/MAPK6 controls IL-8 production and chemotaxis

2020

ERK3 is a ubiquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physiological significance of its short half-life remains unclear. By employing gastrointestinal 3D organoids, we detect that ERK3 protein levels steadily decrease during epithelial differentiation. ERK3 is not required for 3D growth of human gastric epithelium. However, ERK3 is stabilized and activated in tumorigenic cells, but deteriorates over time in primary cells in response to lipopolysaccharide (LPS). ERK3 is necessary for production of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells. Particularly, ERK3 is critical for AP-1 signaling…

0301 basic medicineMAPK/ERK pathwayMouseQH301-705.5ScienceERK3General Biochemistry Genetics and Molecular BiologyCell Line03 medical and health sciencesMice0302 clinical medicineOrganoidmetastasisAnimalsHumansInterleukin 8Biology (General)chemotaxisMitogen-Activated Protein Kinase 6Gene knockdownGeneral Immunology and MicrobiologyIL-8ChemistryKinaseGeneral NeuroscienceQInterleukin-8RChemotaxisGeneral MedicineCell BiologyMAPKgastrointestinal organoidsIn vitroCell biologysecretomeChemotaxis Leukocyte030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMedicineHeterograftsSignal transductionsignal transductionResearch ArticleHumaneLife
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