2025
Redundancy of the OST catalytic subunit facilitates therapeutic targeting of N-glycosylation
Baro M, Lee H, Kelley V, Lou R, Phoomak C, Politi K, Zeiss C, Van Zandt M, Contessa J. Redundancy of the OST catalytic subunit facilitates therapeutic targeting of N-glycosylation. Cell Chemical Biology 2025, 32: 839-853.e6. PMID: 40494352, DOI: 10.1016/j.chembiol.2025.05.005.Peer-Reviewed Original ResearchConceptsN-glycosylationTrafficking of cell surface receptorsInhibits N-glycosylationCell surface receptorsGlycan synthesisCatalytic subunitOligosaccharyltransferaseEnzymatic activitySurface receptorsSTT3BSTT3ACharacterized in vitroDownstream effectsLung cancer xenograftsTherapeutic targetPatient-derivedBiological activityTumor regressionCancer xenograftsSmall moleculesGrowth delayTherapeutic agentsGlycansThe role of long non-coding ribonucleic acid HOXA11-AS in endometriosis therapy
Mamillapalli R, Gawde N, Fay M, Atwani R, Moridi I, Taylor H. The role of long non-coding ribonucleic acid HOXA11-AS in endometriosis therapy. Reproductive Biology And Endocrinology 2025, 23: 83. PMID: 40457415, PMCID: PMC12128536, DOI: 10.1186/s12958-025-01420-0.Peer-Reviewed Original ResearchMeSH KeywordsAdultCell LineCell ProliferationEndometriosisEndometriumFemaleHomeodomain ProteinsHumansProgestinsRNA, Long NoncodingConceptsHOXA11-ASHOXA11-AS expressionEutopic endometriumLong non-coding RNAsEctopic endometriotic lesionsEndometriotic cell linesInvasion of endometriosisEndometrial stromal cellsReal-time polymerase chain reactionNon-coding RNAsEndometriotic lesionsEndometriosis therapyEndometriosis patientsNormal endometriumProgestin responsivenessEndometrial developmentTreatment responsePolymerase chain reactionQuantitative real-time polymerase chain reactionEndometriosisEndometriosis treatmentMethodsTissue samplesStromal cellsPotential target genesEndometriumC/EBPβ increases tumor aggressiveness by enhancing KIFC1 expression in androgen receptor negative triple negative breast cancer
Joshi S, Garlapati C, Nguyen T, Sharma S, Chandrashekar D, Bhattarai S, Varambally S, Krishnamurti U, Li X, Aneja R. C/EBPβ increases tumor aggressiveness by enhancing KIFC1 expression in androgen receptor negative triple negative breast cancer. Cell Communication And Signaling 2025, 23: 255. PMID: 40448099, PMCID: PMC12125945, DOI: 10.1186/s12964-025-02243-7.Peer-Reviewed Original ResearchConceptsHuman epidermal growth factor receptor 2Expression of estrogen receptorAndrogen receptorAggressive characteristicsEpithelial-mesenchymal transitionProgesterone receptorPoor prognosisBreast cancerLack of AR expressionQuadruple-negative breast cancerEpidermal growth factor receptor 2Triple-negative breast tumorsKIFC1 expressionTriple negative breast cancerExpression of therapeutic targetsReduced tumor volumeTherapeutic targetNegative breast cancerRisk predictive biomarkersPromote epithelial-mesenchymal transitionExpression of KIFC1Cancer cell proliferationTumor volumeAR expressionTumor aggressivenessProliferative arrest induces neuronal differentiation and innate immune responses in normal and Creutzfeldt-Jakob Disease agent (CJ) infected rat septal neurons
Pagano N, Perez G, Garcia-Milian R, Manuelidis L. Proliferative arrest induces neuronal differentiation and innate immune responses in normal and Creutzfeldt-Jakob Disease agent (CJ) infected rat septal neurons. PLOS ONE 2025, 20: e0323825. PMID: 40434970, PMCID: PMC12118874, DOI: 10.1371/journal.pone.0323825.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCell ProliferationCreutzfeldt-Jakob SyndromeHumansImmunity, InnateNeuronsRatsConceptsSeptal neuronsInnate immune responseDifferential transcriptionCreutzfeldt-Jakob disease agentCJ infectionImmune responseBind misfolded proteinsInnate immune genesIntestinal myeloid cellsRat septal neuronsArrests normal cellsDisease agentsInnate immune transcriptsCreutzfeldt-JakobModel of latent infectionAnti-viral responseCDNA libraryUnique transcriptsPeripheral human bloodLate-onset diseaseUninfected neuronsUpregulated interferonImmune genesMyeloid cellsTranscriptionIndole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
Zhou S, Wang K, Huang J, Xu Z, Yuan Q, Liu L, Wang Z, Miao J, Wang H, Wang T, Guan W, Ding C. Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming. Gut Microbes 2025, 17: 2508949. PMID: 40409349, PMCID: PMC12118437, DOI: 10.1080/19490976.2025.2508949.Peer-Reviewed Original ResearchConceptsIndole-3-lactic acidColorectal cancer patientsColorectal cancerAryl hydrocarbon receptorDownregulated glucose metabolismPotential clinical therapeutic targetsAnti-apoptotic capabilityInfluence tumor progressionGut microbiota metabolismTumor cell proliferationMetagenomic sequencingPhosphorylation sitesXenograft mouse modelGut microbiotaClinical therapeutic targetMetabolic reprogrammingMicrobiota metabolismP-STAT3Tumor progressionTumor malignancyMouse modelTryptophan metabolismCancer cellsIn vitro experimentsCRC developmentPartial mitochondrial involvement in the antiproliferative and immunostimulatory effects of PT-112
Soler-Agesta R, Beltrán-Visiedo M, Sato A, Yamazaki T, Guilbaud E, Yim C, Congenie M, Ames T, Anel A, Galluzzi L. Partial mitochondrial involvement in the antiproliferative and immunostimulatory effects of PT-112. OncoImmunology 2025, 14: 2507245. PMID: 40386940, PMCID: PMC12091903, DOI: 10.1080/2162402x.2025.2507245.Peer-Reviewed Original ResearchConceptsImmunogenic cell deathTS/A cellsPD-L1Immune checkpoint inhibitorsExposure of calreticulinLigand PD-L1Type I IFN secretionSecrete type I IFNsRelease of HMGB1MHC class IMHC class I moleculesClass I moleculesType I IFNImmunostimulatory signalsCheckpoint inhibitorsCell surfaceTreatment discontinuationClinical responsePreclinical modelsMalignant cellsSolid tumorsTumor typesColorectal carcinomaGenetic alterationsHMGB1 releaseMitochondrial gene SLC25A24 regulated anti-tumor immunity and inhibited the proliferation and metastasis of colorectal cancer by PKG1-dependent cGMP/PKG1 pathway
Gao Y, Peng Y, Zhou Y, Zhu J, Fu S, Chen Y, Cai C, Han Y, Shen H, Zeng S, Mao L, Xiao Z. Mitochondrial gene SLC25A24 regulated anti-tumor immunity and inhibited the proliferation and metastasis of colorectal cancer by PKG1-dependent cGMP/PKG1 pathway. International Immunopharmacology 2025, 157: 114664. PMID: 40334626, DOI: 10.1016/j.intimp.2025.114664.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsAnti-tumor immunityColorectal cancerResponse to immune checkpoint inhibitorsAssociated with worse overall survivalKaplan-Meier survival analysisProgression-free survivalTumor immune regulationMetastasis of colorectal cancerMitochondrial solute carriersMicrosatellite instabilityColorectal cancer cell linesColorectal cancer patientsCancer-related mortalityProliferation-related markersCheckpoint inhibitorsColorectal cancer progressionOverall survivalImmune infiltrationPotential therapeutic targetPrognostic markerUnfavorable prognosisColorectal cancer tissuesImmune regulationClinical cohortGlomerular mesangial cells derived complement factor H regulates complement activation, influences cell proliferation, and maintains actin cytoskeleton
Li Y, Ni X, Li X, Kang Y, Yuan X, Xu G, Wang T, Li D, Shi S, Lv J, Zhao M, Zhang H, Zhu L. Glomerular mesangial cells derived complement factor H regulates complement activation, influences cell proliferation, and maintains actin cytoskeleton. International Immunopharmacology 2025, 154: 114544. PMID: 40157080, DOI: 10.1016/j.intimp.2025.114544.Peer-Reviewed Original ResearchConceptsActin cytoskeletonGlomerular mesangial cellsInfluence cell proliferationCell proliferationSingle-cell sequencing dataComplement factor HNon-canonical functionsExpression of Cdc42Mesangial cellsSequence dataCell motilityAffecting cell proliferationCytoskeletonRegulate complement activationRegulatory roleCanonical functionActinComplement activationIndependent of complement activationFactor HIgA1-containing immune complexesComplement proteinsCellsComplement-induced damageExpressionAn in vivo screen identifies NAT10 as a master regulator of brain metastasis
Chen J, Xu P, Cai W, Chen H, Wingrove E, Shi X, Li W, Biancon G, Zhang M, Balabaki A, Krop E, Asare E, Zhang Y, Yin M, Tebaldi T, Meier J, Westbrook T, Halene S, Liu Y, Shen H, Nguyen D, Yan Q. An in vivo screen identifies NAT10 as a master regulator of brain metastasis. Science Advances 2025, 11: eads6021. PMID: 40138393, PMCID: PMC11939035, DOI: 10.1126/sciadv.ads6021.Peer-Reviewed Original ResearchConceptsPhosphoserine aminotransferase 1Metastasis in vivoIn vivo screeningRNA helicase domainRegulator of brain metastasisMetastatic breast cancer cellsBrain metastasis in vivoBrain metastasesRNA helicaseCell growth in vitroBreast cancer cellsCancer cell proliferationSerine biosynthesisEpigenetic regulationGrowth in vitroNAT10Migration in vitroCancer cellsTumor growthCell proliferationPrimary tumor growthDrivers of brain metastasesRNACancer metastasisCancer-related deathsOuter radial glia promotes white matter regeneration after neonatal brain injury
Jinnou H, Rosko L, Yamashita S, Henmi S, Prasad J, Lam V, Agaronyan A, Tu T, Imamura Y, Kuboyama K, Sawamoto K, Hashimoto-Torii K, Ishibashi N, Gallo V. Outer radial glia promotes white matter regeneration after neonatal brain injury. Cell Reports Medicine 2025, 6: 101986. PMID: 40023165, PMCID: PMC11970391, DOI: 10.1016/j.xcrm.2025.101986.Peer-Reviewed Original ResearchConceptsOuter radial gliaActivating transcription factor 5Oligodendrocyte precursor cellsTreating white matter injuryNeonatal brain injuryWhite matter injuryPeriventricular white matterWhite matter regenerationImprove functional recoveryPopulation of neural stem cellsNeural stem cellsBrain injuryOuter subventricular zoneSubventricular zoneProliferative capacityPostnatal developmentVentricular zoneFunctional recoveryPrecursor cellsStem cellsWhite matterRadial gliaTherapeutic targetNeonatal pigletsInjuryAn Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment
Gao D, Shipman W, Sun Y, Yang W, Mathew A, Beraki L, Glahn J, Kochen A, Kyriakides T, Horsley V, Hsia H. An Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment. ACS Applied Bio Materials 2025, 8: 1675-1683. PMID: 39886738, DOI: 10.1021/acsabm.4c01853.Peer-Reviewed Original ResearchMeSH KeywordsAlginatesAnimalsBiocompatible MaterialsCell ProliferationCollagenFibroblastsFibronectinsHumansHydrogelsMaterials TestingMiceParticle SizeConceptsEncapsulated fibroblastsAlginate hydrogelNeat alginate hydrogelsComposite hydrogelsModified hydrogelsInjectable hydrogelsStorage modulusMechanical propertiesCollagen hydrogelsMacroporous structureHydrogelsPore sizeAlginate functionalizationAlginate controlAlginate matrixAlginateFibroblast behaviorPro-angiogenic potentialFibroblast spreadingModulusPromote wound healingPoreFormation of fibrilsSLC25A38 is required for mitochondrial pyridoxal 5’-phosphate (PLP) accumulation
Pena I, Shi J, Chang S, Yang J, Block S, Adelmann C, Keys H, Ge P, Bathla S, Witham I, Sienski G, Nairn A, Sabatini D, Lewis C, Kory N, Vander Heiden M, Heiman M. SLC25A38 is required for mitochondrial pyridoxal 5’-phosphate (PLP) accumulation. Nature Communications 2025, 16: 978. PMID: 39856062, PMCID: PMC11760969, DOI: 10.1038/s41467-025-56130-3.Peer-Reviewed Original ResearchConceptsPyridoxal 5'-phosphateGenome-wide CRISPR interference screenPyridoxal 5'-phosphate-dependent enzymeCRISPR interference screenSerine hydroxymethyltransferase-2Active form of vitamin B6One-carbon unitsImpaired cellular proliferationAmino acid metabolismOne-carbon metabolismInterference screenEssential proteinsMolecular machineryNucleotide synthesisCongenital sideroblastic anemiaProliferation defectSLC25A38Acid metabolismErythroleukemia cellsOrnithine aminotransferaseActive formK562 cellsEnzymatic reactionsCellular proliferationPolyamine synthesisSignificance of birth in the maintenance of quiescent neural stem cells
Kawase K, Nakamura Y, Wolbeck L, Takemura S, Zaitsu K, Ando T, Jinnou H, Sawada M, Nakajima C, Rydbirk R, Gokenya S, Ito A, Fujiyama H, Saito A, Iguchi A, Kratimenos P, Ishibashi N, Gallo V, Iwata O, Saitoh S, Khodosevich K, Sawamoto K. Significance of birth in the maintenance of quiescent neural stem cells. Science Advances 2025, 11: eadn6377. PMID: 39841848, PMCID: PMC11753423, DOI: 10.1126/sciadv.adn6377.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBrainCell ProliferationEpendymoglial CellsFemaleGlutamineMiceNeural Stem CellsNeurogenesisParturitionConceptsNeural stem cellsQuiescent neural stem cellsStem cellsRadial gliaNeural stem cell poolAcquisition of quiescenceEmbryonic neural stem cellsPreterm birthPostnatal neural stem cellsCellular processesPostnatal neurogenesisGlutamine metabolismPostnatal brainLong-term maintenanceDevelopmental processesBirthNeurogenesisPretermCells
2024
Development of a small molecule-based two-photon photosensitizer for targeting cancer cells
Lee D, Cao Y, Juvekar V, Sauraj, Noh C, Shin S, Liu Z, Kim H. Development of a small molecule-based two-photon photosensitizer for targeting cancer cells. Journal Of Materials Chemistry B 2024, 12: 12232-12238. PMID: 39469993, DOI: 10.1039/d4tb01706d.Peer-Reviewed Original ResearchConceptsTarget cancer cellsReactive oxygen speciesPhotodynamic therapyCancer cellsDiverse cell linesInduced ROS productionColon cancer tissuesTwo-photon (TPCell deathLow dark toxicityCancer modelsTwo-photon photosensitizerROS productionCancer selectivityInduce cell damageThree-dimensional spheroidsCell linesTP excitationImaging-guided photodynamic therapyCancer tissuesOxygen speciesTP-PDTEzrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktA proteogenomic analysis of cervical cancer reveals therapeutic and biological insights
Yu J, Gui X, Zou Y, Liu Q, Yang Z, An J, Guo X, Wang K, Guo J, Huang M, Zhou S, Zuo J, Chen Y, Deng L, Yuan G, Li N, Song Y, Jia J, Zeng J, Zhao Y, Liu X, Du X, Liu Y, Wang P, Zhang B, Ding L, Robles A, Rodriguez H, Zhou H, Shao Z, Wu L, Gao D. A proteogenomic analysis of cervical cancer reveals therapeutic and biological insights. Nature Communications 2024, 15: 10114. PMID: 39578447, PMCID: PMC11584810, DOI: 10.1038/s41467-024-53830-0.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAdultBiomarkers, TumorCell Line, TumorCell ProliferationE1A-Associated p300 ProteinFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedPapillomaviridaePapillomavirus InfectionsPrognosisProtein Kinase C betaProtein Processing, Post-TranslationalProteogenomicsProto-Oncogene Proteins c-fosUterine Cervical NeoplasmsConceptsCervical cancerIncidence of cervical cancerIntegrative proteogenomic analysisMulti-omic changesHuman papillomavirusImmune infiltrationSignificant public health issueProteogenomic analysisGenetic alterationsCC patientsPatient subgroupsMalignant proliferationAnalysis of cervical cancerCC tumorsChinese womenPost-translational modifications regulationPublic health issuePotential treatmentScreening strategiesClinical practiceProliferation of CC cellsPatientsWomen's healthCancerLow-income countriesG9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1
Exposito F, Redrado M, Serrano D, Calabuig-Fariñas S, Bao-Caamano A, Gallach S, Jantus-Lewintre E, Diaz-Lagares A, Rodriguez-Casanova A, Sandoval J, San Jose-Eneriz E, Garcia J, Redin E, Senent Y, Leon S, Pio R, Lopez R, Oyarzabal J, Pineda-Lucena A, Agirre X, Montuenga L, Prosper F, Calvo A. G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1. Cell Death & Disease 2024, 15: 787. PMID: 39488528, PMCID: PMC11531574, DOI: 10.1038/s41419-024-07156-w.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerNon-small cell lung cancer patientsCM-272Treatment of non-small cell lung cancerReprogram tumor cellsAssociated with poor prognosisResponse to chemotherapyCell lung cancerCancer drugsMonitor tumor progressionOverexpression of G9aNSCLC cell linesLung cancer growthCancer drug sensitivityNon-small cell lung cancer growthNon-invasive biomarkersTumor volumeAntitumor efficacyTargeted therapyPoor prognosisCancer modelsTumor cellsInduce cell deathTumor progressionLung cancerMitochondrial reprogramming by activating OXPHOS via glutamine metabolism in African American patients with bladder cancer
Reddy K, Piyarathna D, Park J, Putluri V, Amara C, Kamal A, Xu J, Kraushaar D, Huang S, Jung S, Eberlin L, Johnson J, Kittles R, Ballester L, Parsawar K, Siddiqui M, Gao J, Gramer A, Bollag R, Terris M, Lotan Y, Creighton C, Lerner S, Sreekumar A, Kaipparettu B, Putluri N. Mitochondrial reprogramming by activating OXPHOS via glutamine metabolism in African American patients with bladder cancer. JCI Insight 2024, 9: e172336. PMID: 39253977, PMCID: PMC11385078, DOI: 10.1172/jci.insight.172336.Peer-Reviewed Original ResearchConceptsBladder cancerOxidative phosphorylationComponents of complex IComplex IElevated mitochondrial oxidative phosphorylationComprehensive RNA-seqReduced basal respirationActive oxidative phosphorylationMitochondrial oxidative phosphorylationDecreased tumor growthTumor growth potentialIncreased disease progressionMitochondrial respiration rateAfrican American patientsRNA-seqRace-specific differencesMitochondrial reprogrammingEuropean AmericansMetabolic rewiringOXPHOS activityBasal respirationGlutamine metabolismGLS1 expressionPreclinical studiesATP productionPreclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer
Hartwich T, Mansolf M, Demirkiran C, Greenman M, Bellone S, McNamara B, Nandi S, Alexandrov L, Yang‐Hartwich Y, Coma S, Pachter J, Santin A. Preclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer. Cancer Medicine 2024, 13: e70210. PMID: 39240189, PMCID: PMC11378359, DOI: 10.1002/cam4.70210.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCarcinoma, EndometrioidCell Line, TumorCell ProliferationEndometrial NeoplasmsExome SequencingFemaleFocal Adhesion Kinase 1HumansImidazolesMiceNeoplasm GradingOxazepinesProtein Kinase InhibitorsPyrazinesSulfonamidesXenograft Model Antitumor AssaysConceptsFocal adhesion kinaseWhole-exome sequencingEndometrial cancer cell linesVS-4718Cell linesRas/MAPK pathwayPhosphorylated focal adhesion kinaseWestern blot assayWhole-exome sequencing resultsRAF/MEK inhibitionEAC cell linesBlot assayP-FAKGenetic landscapeCell cycleEndometrial cancerGenetic derangementsDefactinibP-MEKGrowth inhibitionRAF/MEKRas/MAPKCell viabilityP-ERKHigh-grade endometrial cancerStatins Inhibit Cutaneous Squamous Cell Carcinoma Cells
HACKETT A, COHEN A, RUTENBERG T, HODAK E, MOYAL L, ATZMONY L. Statins Inhibit Cutaneous Squamous Cell Carcinoma Cells. Acta Dermato Venereologica 2024, 104: 25097. PMID: 39185545, PMCID: PMC11367778, DOI: 10.2340/actadv.v104.25097.Peer-Reviewed Original Research
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