2024
Class Effect Unveiled: PPARγ Agonists and MEK Inhibitors in Cancer Cell Differentiation
Ben-Yishay R, Globus O, Balint-Lahat N, Arbili-Yarhi S, Bar-Hai N, Bar V, Aharon S, Kosenko A, Zundelevich A, Berger R, Ishay-Ronen D. Class Effect Unveiled: PPARγ Agonists and MEK Inhibitors in Cancer Cell Differentiation. Cells 2024, 13: 1506. PMID: 39273076, PMCID: PMC11394433, DOI: 10.3390/cells13171506.Peer-Reviewed Original ResearchConceptsMEK inhibitorsBreast cancer cellsEpithelial-to-mesenchymal transitionCancer cellsPPARg agonistsDrug resistanceTherapeutic approachesTriple-negative breast cancerMurine breast cancer cellsAggressive breast cancer subtypeDevelopment of drug resistanceCancer cell plasticityBreast cancer subtypesCombination of pioglitazoneOvercome drug resistanceDedifferentiated cancer cellsBreast cancer progressionCancer cell differentiationCytoskeleton rearrangementLipid droplet accumulationCell trans-differentiationBreast cancerCancer subtypesCell plasticityTherapeutic strategiesNuclear PKM2 binds pre-mRNA at folded G-quadruplexes and reveals their gene regulatory role
Anastasakis D, Apostolidi M, Garman K, Polash A, Umar M, Meng Q, Scutenaire J, Jarvis J, Wang X, Haase A, Brownell I, Rinehart J, Hafner M. Nuclear PKM2 binds pre-mRNA at folded G-quadruplexes and reveals their gene regulatory role. Molecular Cell 2024, 84: 3775-3789.e6. PMID: 39153475, PMCID: PMC11455610, DOI: 10.1016/j.molcel.2024.07.025.Peer-Reviewed Original ResearchRNA-binding proteinsPre-mRNANon-canonical RNA-binding proteinsGene regulatory roleCancer cellsRNA G-quadruplexesG-quadruplexInvasion of cancer cellsTriple-negative breast cancer cellsBreast cancer cellsEpithelial-to-mesenchymal transitionCancer typesNuclear localizationPrecursor mRNANuclear accumulationGene expressionXenograft mouse modelNuclear PKM2Regulatory roleRG4sPKM2Reduced migrationMouse modelTumor progressionPatient survivalProgestogen-driven B7-H4 contributes to onco-fetal immune tolerance
Yu J, Yan Y, Li S, Xu Y, Parolia A, Rizvi S, Wang W, Zhai Y, Xiao R, Li X, Liao P, Zhou J, Okla K, Lin H, Lin X, Grove S, Wei S, Vatan L, Hu J, Szumilo J, Kotarski J, Freeman Z, Skala S, Wicha M, Cho K, Chinnaiyan A, Schon S, Wen F, Kryczek I, Wang S, Chen L, Zou W. Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance. Cell 2024, 187: 4713-4732.e19. PMID: 38968937, PMCID: PMC11344674, DOI: 10.1016/j.cell.2024.06.012.Peer-Reviewed Original ResearchB7-H4Immune toleranceProgesterone receptorCD8<sup>+</sup> T cell exhaustionImmune tolerance checkpointB7-H4 expressionT cell exhaustionImmune tolerance mechanismsMaternal-fetal interfaceBreast cancer modelFemale sex hormonesBreast cancer progressionBreast cancer cellsTolerance checkpointsFetal resorptionHuman cancer typesHormonal screeningImmune activationPregnancy modelCancer modelsSex hormonesCell exhaustionPR antagonistsGenetic deficiencyCancer cellsNCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells
Sánchez J, Alemán A, Henao J, Olaya J, Ehrlich B. NCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells. Journal Of Physiology And Biochemistry 2024, 80: 451-463. PMID: 38564162, PMCID: PMC11074019, DOI: 10.1007/s13105-024-01016-z.Peer-Reviewed Original ResearchConceptsTransient receptor potential channel ankyrin 1Breast cancerPI3K pathwayNCS-1Chemotherapy-induced peripheral neuropathyCa2+ channelsK pathwayCa2+ influxNCS-1 expressionBreast cancer cellsCa2+ sensorCa2+ homeostasisCa2+ dynamicsNeuronal calcium sensor-1MDA-MB-231Fura-2Open probabilityPain sensationAnkyrin 1Peripheral neuropathyTRPA1 channelsCo-immunoprecipitationChannel functionRegulatory componentsCellular pathwaysUnique Spatial Transcriptomic Profiling of the Murine Femoral Fracture Callus: A Preliminary Report
Jiang W, Caruana D, Back J, Lee F. Unique Spatial Transcriptomic Profiling of the Murine Femoral Fracture Callus: A Preliminary Report. Cells 2024, 13: 522. PMID: 38534368, PMCID: PMC10969736, DOI: 10.3390/cells13060522.Peer-Reviewed Original ResearchConceptsMDA-MB-231Transcriptomic platformsGene expressionSpatially localized gene expressionMDA-MB-231 metastatic breast cancer cellsSpatial transcriptomics platformGenetic expression changesFracture healingMetastatic breast cancer cellsBreast cancer cellsImpaired fracture healingSingle-cell RNALocal gene expressionSpatial transcriptomic profilingFracture callus formationGenomic heterogeneitySequencing techniquesDisrupt bone homeostasisTranscriptome profilingIn situ hybridizationExpression changesSoft callusPathological fracturesWild-typeSpatial transcriptomics
2023
5-Azacytidine- and retinoic-acid-induced reprogramming of DCCs into dormancy suppresses metastasis via restored TGF-β-SMAD4 signaling
Singh D, Carcamo S, Farias E, Hasson D, Zheng W, Sun D, Huang X, Cheung J, Nobre A, Kale N, Sosa M, Bernstein E, Aguirre-Ghiso J. 5-Azacytidine- and retinoic-acid-induced reprogramming of DCCs into dormancy suppresses metastasis via restored TGF-β-SMAD4 signaling. Cell Reports 2023, 42: 112560. PMID: 37267946, PMCID: PMC10592471, DOI: 10.1016/j.celrep.2023.112560.Peer-Reviewed Original ResearchConceptsDisseminated cancer cellsCancer cellsDNA methylation inhibitorNon-proliferative stateAnti-proliferative functionTranscriptional reprogrammingChromatin remodelingRetinoic acid receptorsTranscriptional programsMethylation inhibitorGrowth factor βMicroenvironmental signalsSMAD4 knockdownBreast cancer cellsDormancySuppress metastasisRARα-specific agonistLung metastasis formationNeck squamous cell carcinomaReprogrammingRetinoic acidSquamous cell carcinomaTrans retinoic acidFactor βMetastasis formation
2022
Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the F1FO ATP synthase
Park HA, Brown SR, Jansen J, Dunn T, Scott M, Mnatsakanyan N, Jonas EA, Kim Y. Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the F1FO ATP synthase. Biochemical And Biophysical Research Communications 2022, 632: 173-180. PMID: 36209586, PMCID: PMC10024463, DOI: 10.1016/j.bbrc.2022.09.084.Peer-Reviewed Original ResearchHuman WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation
Cai WL, Chen JF, Chen H, Wingrove E, Kurley SJ, Chan LH, Zhang M, Arnal-Estape A, Zhao M, Balabaki A, Li W, Yu X, Krop ED, Dou Y, Liu Y, Jin J, Westbrook TF, Nguyen DX, Yan Q. Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation. ELife 2022, 11: e78163. PMID: 36043466, PMCID: PMC9584608, DOI: 10.7554/elife.78163.Peer-Reviewed Original ResearchConceptsBreast cancer cellsMetastatic breast cancerBreast cancerRibosomal gene expressionCancer cellsKnockdown of WDR5Vivo genetic screenReversible epigenetic mechanismsGenetic screenTranslation regulationTriple-negative breast cancerEpigenetic regulatorsEpigenetic mechanismsBreast cancer growthCancer-related deathTranslation efficiencyWDR5Novel therapeutic strategiesTranslation rateGene expressionCell growthAdvanced diseaseEffective therapyMetastatic capabilityPotent suppressionRedox regulation of RAD51 Cys319 and homologous recombination by peroxiredoxin 1
Skoko J, Cao J, Gaboriau D, Attar M, Asan A, Hong L, Paulsen C, Ma H, Liu Y, Wu H, Harkness T, Furdui C, Manevich Y, Morrison C, Brown E, Normolle D, Spies M, Spies M, Carroll K, Neumann C. Redox regulation of RAD51 Cys319 and homologous recombination by peroxiredoxin 1. Redox Biology 2022, 56: 102443. PMID: 36058112, PMCID: PMC9450138, DOI: 10.1016/j.redox.2022.102443.Peer-Reviewed Original ResearchConceptsRAD51 foci formationFoci formationRedox regulationHomologous recombination DNA repair pathwayHR DNA repairProtein binding partnersPoly (ADP-ribose) polymeraseDNA repair pathwaysDAz-2Rad51 proteinSensitization of cellsRad51 filamentsBinding partnerHomologous recombinationDNA repairCysteine oxidationRepair pathwaysMediator proteinsHuman breast cancer cellsCellular responsesPeroxiredoxin 1Breast cancer cellsDNA damagePRDX1Cys319Dual-targeted enzyme-sensitive hyaluronic acid nanogels loading paclitaxel for the therapy of breast cancer
Gao D, Asghar S, Ye J, Zhang M, Hu R, Wang Y, Huang L, Yuan C, Chen Z, Xiao Y. Dual-targeted enzyme-sensitive hyaluronic acid nanogels loading paclitaxel for the therapy of breast cancer. Carbohydrate Polymers 2022, 294: 119785. PMID: 35868795, DOI: 10.1016/j.carbpol.2022.119785.Peer-Reviewed Original ResearchConceptsBreast cancerHyaluronic acid nanogelsTumor-bearing BALB/c miceTherapy of breast cancerTreatment of breast cancerTargeting breast cancerBreast cancer cellsRat pharmacokinetic profilesIn vivo studiesTherapeutic efficacyBALB/c miceEntrapment efficiencyPharmacokinetic profileCancer cellsClearance rateCD44 receptorControl groupCancerPaclitaxelDrug loadingHigher cytotoxicityReceptorsCD44DrugCellsMicrotentacle Formation in Ovarian Carcinoma
Reader JC, Fan C, Ory EC, Ju J, Lee R, Vitolo MI, Smith P, Wu S, Ching MMN, Asiedu EB, Jewell CM, Rao GG, Fulton A, Webb TJ, Yang P, Santin AD, Huang HC, Martin SS, Roque DM. Microtentacle Formation in Ovarian Carcinoma. Cancers 2022, 14: 800. PMID: 35159067, PMCID: PMC8834106, DOI: 10.3390/cancers14030800.Peer-Reviewed Original ResearchHuman ovarian surface epitheliumOvarian cancerCell linesCancer cellsMajor therapeutic challengeIntraperitoneal drug deliveryOvarian surface epitheliumOvarian cancer metastasisNew therapeutic targetsDevelopment of chemoresistanceEffect of treatmentBreast cancer cellsOSC cell linesExtrapelvic metastasesMalignant ascitesTherapeutic challengeOvarian carcinomaSurface epitheliumTherapeutic targetMetastatic potentialAscitesCancer metastasisΒ-tubulin isotypesIndividual cancer cellsMetastasisAntiproliferative effects of olanzapine against MCF-7 human breast cancer cells and its molecular interactions with surviving
Nuthalapati P. Antiproliferative effects of olanzapine against MCF-7 human breast cancer cells and its molecular interactions with surviving. Brain Tumor Research And Treatment 2022, 10: s141. DOI: 10.14791/btrt.2022.10.f-2510.Peer-Reviewed Original Research
2021
MAL2 mediates the formation of stable HER2 signaling complexes within lipid raft-rich membrane protrusions in breast cancer cells
Jeong J, Shin JH, Li W, Hong JY, Lim J, Hwang JY, Chung JJ, Yan Q, Liu Y, Choi J, Wysolmerski J. MAL2 mediates the formation of stable HER2 signaling complexes within lipid raft-rich membrane protrusions in breast cancer cells. Cell Reports 2021, 37: 110160. PMID: 34965434, PMCID: PMC8762588, DOI: 10.1016/j.celrep.2021.110160.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Agents, ImmunologicalBreast NeoplasmsCell ProliferationCytoskeletal ProteinsDrug Resistance, NeoplasmEndocytosisFemaleHumansMembrane MicrodomainsMyelin and Lymphocyte-Associated Proteolipid ProteinsPhosphoproteinsPlasma Membrane Calcium-Transporting ATPasesReceptor, ErbB-2Sodium-Hydrogen ExchangersTrastuzumabTumor Cells, CulturedConceptsLipid raft formationBreast cancer cellsLipid raftsLipid raft resident proteinsCancer cellsRaft formationRaft-resident proteinsProximity ligation assayProtein complexesMembrane protrusionsProtein interactionsPlasma membraneLigation assayMAL2Membrane stabilityStructural organizationPotential therapeutic targetPhysical interactionMembrane retentionProteinRaftsTherapeutic targetCellsIntracellular calcium concentrationLow intracellular calcium concentrationInflammatory conversion of quiescent osteoblasts by metastatic breast cancer cells through pERK1/2 aggravates cancer-induced bone destruction
Back J, Nguyen MN, Li L, Lee S, Lee I, Chen F, Gillinov L, Chung YH, Alder KD, Kwon HK, Yu KE, Dussik CM, Hao Z, Flores MJ, Kim Y, Ibe IK, Munger AM, Seo SW, Lee FY. Inflammatory conversion of quiescent osteoblasts by metastatic breast cancer cells through pERK1/2 aggravates cancer-induced bone destruction. Bone Research 2021, 9: 43. PMID: 34588427, PMCID: PMC8481290, DOI: 10.1038/s41413-021-00158-w.Peer-Reviewed Original ResearchCancer-induced bone destructionBreast cancer cellsOsteolytic breast cancerBone homeostasisCancer growthCancer cellsBone destructionInflammatory osteolysisBreast cancerBreast cancer-induced bone destructionOsteolytic breast cancer metastasesPromising adjuvant therapyERK1/2 activationMEK1 expressionBreast cancer metastasisMetastatic breast cancer cellsActivation of pERK1/2Inflammatory conversionAdjuvant therapyPathological fracturesHuman pathological specimensBone microenvironmentPathological specimensSkeletal diseasePathway inhibitorReactivation of tumour suppressor in breast cancer by enhancer switching through NamiRNA network
Liang Y, Lu Q, Li W, Zhang D, Zhang F, Zou Q, Chen L, Tong Y, Liu M, Wang S, Li W, Ren X, Xu P, Yang Z, Dong S, Zhang B, Huang Y, Li D, Wang H, Yu W. Reactivation of tumour suppressor in breast cancer by enhancer switching through NamiRNA network. Nucleic Acids Research 2021, 49: 8556-8572. PMID: 34329471, PMCID: PMC8421228, DOI: 10.1093/nar/gkab626.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCarcinogenesisDNA MethylationEnhancer Elements, GeneticEpigenomicsFemaleGene Expression Regulation, NeoplasticGene SilencingHumansMicroRNAsPromoter Regions, GeneticReceptors, EstrogenReceptors, G-Protein-CoupledRegulatory Sequences, Nucleic AcidRNA, NeoplasmTumor Suppressor ProteinsConceptsTumor suppressor geneLowest expression of miRNABreast cancerLow expressionDysfunction of tumor suppressor genesLoss of function of tumor suppressor genesTriple negative breast cancer subtypeCancer developmentFunction of tumor suppressor genesMiR-339Inactivation of tumor suppressor genesClinical breast cancer treatmentTumor suppressor gene inactivationExpression of miRNAsReactivation of tumor suppressor genesBreast cancer subtypesBreast cancer cellsBreast cancer treatmentLuminal A/BPaired breast cancerAberrant histone modificationsGPER1 expressionEpigenetic abnormalitiesCancer subtypesSuppressor geneAutocrine GMCSF Signaling Contributes to Growth of HER2+ Breast Leptomeningeal CarcinomatosisGMCSF Contributes to Breast Leptomeningeal Carcinomatosis
Ansari K, Bhan A, Saotome M, Tyagi A, De Kumar B, Chen C, Takaku M, Jandial R. Autocrine GMCSF Signaling Contributes to Growth of HER2+ Breast Leptomeningeal CarcinomatosisGMCSF Contributes to Breast Leptomeningeal Carcinomatosis. Cancer Research 2021, 81: 4723-4735. PMID: 34247146, PMCID: PMC8986153, DOI: 10.1158/0008-5472.can-21-0259.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutocrine CommunicationBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalGene ExpressionGranulocyte-Macrophage Colony-Stimulating FactorHumansMeningeal CarcinomatosisMiceOncogene ProteinsProtein Kinase InhibitorsReceptor, ErbB-2Signal TransductionXenograft Model Antitumor AssaysConceptsOligodendrocyte progenitor cellsLeptomeningeal carcinomatosisLC growthPan-Aurora kinase inhibitorKinase inhibitorsSuppression of HER2Growth of HER2Central nervous system cell typesProliferation of HER2Nervous system cell typesBreast cancer cellsPrimary HER2Targetable axisOminous complicationIntrathecal deliveryMolecular mechanismsTreatment optionsDire prognosisSpinal cordBreast cancerHER2LC developmentLeptomeningesLC/MS-MSCarcinomatosisInduction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases
Zheng W, Zhao D, Zhang H, Chinnasamy P, Sibinga N, Pollard JW. Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases. Wellcome Open Research 2021, 6: 52. PMID: 33824914, PMCID: PMC8008350, DOI: 10.12688/wellcomeopenres.16569.2.Peer-Reviewed Original ResearchGene expression programsDifferent gene expression profilesGene-targeted mouse modelsGene expression profilesFactor 1Interferon-responsive genesAllograft inflammatory factor-1Metastatic breast cancer cellsExpression programsInflammatory factor-1Functional validationExpression profilesActivated pathwaysMetastatic growthC57BL6/J backgroundBreast cancer cellsSignificant enrichmentFunctional relevanceInterferon SignalingResident alveolar macrophagesBreast cancer metastasisQRT-PCRStrong upregulationCancer metastasisHuman macrophagesAlteration of the F1Fo ATP Synthase Causes Metabolic Remodeling in Breast Cancer Cells
Dunn T, Mnatsakanyan N, Brown S, Jansen J, Hayden M, Jonas E, Kim Y, Park H. Alteration of the F1Fo ATP Synthase Causes Metabolic Remodeling in Breast Cancer Cells. Current Developments In Nutrition 2021, 5: 266. PMCID: PMC8182114, DOI: 10.1093/cdn/nzab036_008.Peer-Reviewed Original ResearchATP synthase subunitsF1Fo-ATP synthaseSynthase subunitsATP synthaseFluid shear stressBreast cancer cellsMDA-MB-231 human breast cancer cellsEnergy metabolismCancer cellsMetabolic remodelingHuman breast cancer cellsOxygen consumption rateIntracellular ATPMitochondrial energy metabolismMDA-MB-231 breast cancer cellsMetastatic cancer cellsC subunitCell divisionMitochondrial remodelingMultienzyme complexMDA-MB-231 cellsReactive oxygen speciesIntracellular energy metabolismATP productionActive transport systemInduction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases
Zheng W, Zhao D, Zhang H, Chinnasamy P, Sibinga N, Pollard J. Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases. Wellcome Open Research 2021, 6: 52. DOI: 10.12688/wellcomeopenres.16569.1.Peer-Reviewed Original ResearchGene expression programsDifferent gene expression profilesGene-targeted mouse modelsGene expression profilesFactor 1Interferon-responsive genesAllograft inflammatory factor-1Metastatic breast cancer cellsExpression programsInflammatory factor-1Functional validationExpression profilesActivated pathwaysMetastatic growthC57BL6/J backgroundBreast cancer cellsSignificant enrichmentFunctional relevanceInterferon SignalingResident alveolar macrophagesBreast cancer metastasisQRT-PCRStrong upregulationCancer metastasisHuman macrophagesPhase I study of JAK1/2 inhibitor ruxolitinib with weekly paclitaxel for the treatment of HER2-negative metastatic breast cancer
Lynce F, Williams JT, Regan MM, Bunnell CA, Freedman RA, Tolaney SM, Chen WY, Mayer EL, Partridge AH, Winer EP, Overmoyer B. Phase I study of JAK1/2 inhibitor ruxolitinib with weekly paclitaxel for the treatment of HER2-negative metastatic breast cancer. Cancer Chemotherapy And Pharmacology 2021, 87: 673-679. PMID: 33585999, DOI: 10.1007/s00280-021-04245-x.Peer-Reviewed Original ResearchConceptsHER2-negative metastatic breast cancerMetastatic breast cancerBreast cancerWeekly paclitaxelAdvanced diseaseHormone receptor-positive diseaseTriple-negative breast cancerGrade 4/5 toxicitiesMost frequent toxicitiesPhase 2 doseWeekly paclitaxel 80Receptor-positive diseaseDose-escalation designJAK1/2 inhibitor ruxolitinibCombination of ruxolitinibBreast cancer cellsOral ruxolitinibPaclitaxel 80PurposePreclinical studiesChemotherapy regimensFrequent toxicitiesProtocol therapyMethodsEligible patientsThirteen patientsVisceral disease
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply