2025
QKI-induced circ_0001766 inhibits colorectal cancer progression and rapamycin resistance by miR-1203/PPP1R3C/mTOR/Myc axis
Zhou Y, Gao Y, Peng Y, Cai C, Han Y, Chen Y, Deng G, Ouyang Y, Shen H, Zeng S, Du Y, Xiao Z. QKI-induced circ_0001766 inhibits colorectal cancer progression and rapamycin resistance by miR-1203/PPP1R3C/mTOR/Myc axis. Cell Death Discovery 2025, 11: 192. PMID: 40263288, PMCID: PMC12015279, DOI: 10.1038/s41420-025-02478-w.Peer-Reviewed Original ResearchCRC cell proliferationCircular RNAsCompetitive endogenous RNAColorectal cancer tissuesInhibited CRC cell proliferationColorectal cancer progressionRapamycin resistanceColorectal cancerEndogenous RNADrug resistancePhosphorylation of MycRNA-binding proteinsModulating CRC progressionRate of drug resistanceActivation of mTOR signalingCell proliferationAssociated with patient survivalPre-mRNACircRNAsQKI expressionMYC phosphorylationIntron 1MYC pathwayCRC progressionInduce apoptosis
2024
Mutational signature-based identification of DNA repair deficient gastroesophageal adenocarcinomas for therapeutic targeting
Prosz A, Sahgal P, Huffman B, Sztupinszki Z, Morris C, Chen D, Börcsök J, Diossy M, Tisza V, Spisak S, Likasitwatanakul P, Rusz O, Csabai I, Cecchini M, Baca Y, Elliott A, Enzinger P, Singh H, Ubellaker J, Lazaro J, Cleary J, Szallasi Z, Sethi N. Mutational signature-based identification of DNA repair deficient gastroesophageal adenocarcinomas for therapeutic targeting. Npj Precision Oncology 2024, 8: 87. PMID: 38589664, PMCID: PMC11001913, DOI: 10.1038/s41698-024-00561-6.Peer-Reviewed Original ResearchNucleotide excision repairGastric cancer cell linesNucleotide excision repair-deficientPlatinum chemotherapyHR deficiencyCancer cell linesPARP inhibitorsHomologous recombinationGenome sequence dataSensitivity to platinum chemotherapySingle-cell RNA sequencingCell linesHR-deficient cancersDNA repair pathwaysSensitivity to cisplatinRad51 foci assaysMutational signature analysisSequence dataGenomic featuresWhole exomeInduce apoptosisRNA sequencingGastroesophageal adenocarcinomaRepair pathwaysHRD scoreEGFR targeting PhosTACs as a dual inhibitory approach reveals differential downstream signaling
Hu Z, Chen P, Li W, Krone M, Zheng S, Saarbach J, Velasco I, Hines J, Liu Y, Crews C. EGFR targeting PhosTACs as a dual inhibitory approach reveals differential downstream signaling. Science Advances 2024, 10: eadj7251. PMID: 38536914, PMCID: PMC10971414, DOI: 10.1126/sciadv.adj7251.Peer-Reviewed Original ResearchConceptsInhibit cancer cell viabilityProteome-wide levelCancer cell viabilityDifferential signaling pathwaysPhosphoproteomic approachTyrosine dephosphorylationProtein dephosphorylationSignal transductionActivating dephosphorylationInduce apoptosisReceptor tyrosine kinase inhibitorsRTK activationSignaling pathwayInhibition of kinasesDephosphorylationEpidermal growth factor receptorGrowth factor receptorCell viabilityFactor receptorInhibitory approachesTyrosineTyrosine kinase inhibitorsInhibitory effectInhibitory potentialKinase inhibitorsA synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress
Fedeles B, Bhardwaj R, Ishikawa Y, Khumsubdee S, Krappitz M, Gubina N, Volpe I, Andrade D, Westergerling P, Staudner T, Campolo J, Liu S, Dong K, Cai Y, Rehman M, Gallagher A, Ruchirawat S, Croy R, Essigmann J, Fedeles S, Somlo S. A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317344121. PMID: 38241440, PMCID: PMC10823221, DOI: 10.1073/pnas.2317344121.Peer-Reviewed Original ResearchConceptsCyst cellsAutosomal dominant polycystic kidney diseaseMouse models of autosomal dominant polycystic kidney diseasePolycystic kidney diseaseModel of autosomal dominant polycystic kidney diseaseKidney diseaseDeveloped primersMitochondrial oxidative stressPathophysiology of autosomal dominant polycystic kidney diseaseOxidative stressInduce apoptosisMitochondrial respirationCystic cellsUp-regulating aerobic glycolysisHomozygous inactivationMonogenic causeDominant polycystic kidney diseaseAerobic glycolysisRenal replacement therapyApoptosisEnd-stage kidney diseaseAnti-tumor agentsAdult mouse modelChronic kidney diseaseAlkylate DNA
2015
Pyrvinium selectively targets blast phase-chronic myeloid leukemia through inhibition of mitochondrial respiration
Xiang W, Cheong J, Ang S, Teo B, Xu P, Asari K, Sun W, Than H, Bunte R, Virshup D, Chuah C. Pyrvinium selectively targets blast phase-chronic myeloid leukemia through inhibition of mitochondrial respiration. Oncotarget 2015, 6: 33769-33780. PMID: 26378050, PMCID: PMC4741801, DOI: 10.18632/oncotarget.5615.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsAntigens, CD34Antineoplastic Combined Chemotherapy ProtocolsApoptosisbeta CateninBlast CrisisCasein Kinase ICell Line, TumorCell ProliferationDasatinibHumansInhibitory Concentration 50K562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, SCIDMitochondriaNeoplasm TransplantationPhosphorylationPyrvinium CompoundsRNA InterferenceConceptsChronic phase chronic myeloid leukemiaTyrosine kinase inhibitorsBCR-ABL1 tyrosine kinase inhibitorsMitochondrial respirationInduce apoptosisBP-CMLBlast phaseFDA-approved anthelminthic drugBCR-ABL1Casein kinase 1aMyeloid leukemiaEffects of pyrviniumTargeting mitochondrial respirationInhibition of mitochondrial respirationCD34+ progenitor cellsInhibit mitochondrial respirationBP-CML patientsCD34+ cellsChronic myeloid leukemiaCord blood CD34Inhibited tumor growthSelf-renewal capacityWnt/b-catenin signaling pathwayInhibited colony formationKinase 1A
2014
Sequential Application of a Cytotoxic Nanoparticle and a PI3K Inhibitor Enhances Antitumor Efficacy
Pandey A, Kulkarni A, Roy B, Goldman A, Sarangi S, Sengupta P, Phipps C, Kopparam J, Oh M, Basu S, Kohandel M, Sengupta S. Sequential Application of a Cytotoxic Nanoparticle and a PI3K Inhibitor Enhances Antitumor Efficacy. Cancer Research 2014, 74: 675-685. PMID: 24121494, PMCID: PMC3946433, DOI: 10.1158/0008-5472.can-12-3783.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell SurvivalCisplatinErbB ReceptorsFemaleHumansMiceModels, BiologicalNanoparticlesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReproducibility of ResultsSignal TransductionConceptsMolecular targeted therapeuticsEnhanced antitumor efficacyAntitumor efficacyBreast cancerCytotoxic agents to tumorsPharmacological inhibitor of PI3KImpact of drug sequencingCombination of nanomedicineAgents to tumorsBreast cancer cellsPI3K) pathwayManagement of cancerInhibitor of PI3KCytotoxic nanoparticlesCombination therapyDrug sequenceOncogenic driversAntitumor outcomesProsurvival signalingCancer cellsPharmacological inhibitorsCancer chemotherapyInduce apoptosisCancerIn vivo validation
2013
Transient overexpression of TGFBR3 induces apoptosis in human nasopharyngeal carcinoma CNE-2Z cells
Zheng F, He K, Li X, Zhao D, Sun F, Zhang Y, Nie D, Li X, Chu W, Sun Y, Lu Y. Transient overexpression of TGFBR3 induces apoptosis in human nasopharyngeal carcinoma CNE-2Z cells. Bioscience Reports 2013, 33: e00029. PMID: 23387308, PMCID: PMC3596095, DOI: 10.1042/bsr20120047.Peer-Reviewed Original ResearchConceptsCaspase 3 activityTransient overexpressionBcl-2P-BadCNE-2Z cellsApoptosis-inducing factorCNE-2ZExpression of apoptosis-related proteinsPro-apoptotic BadCaspase 3 pathwayApoptosis-related proteinsCaspase 3 activity kitXIAP proteinBax proteinTime-dependent mannerInduce apoptosisCaspaseForced expressionReduced viabilityPlasmid DNAApoptosisXIAPTGFBR3 overexpressionProteinNasopharyngeal carcinoma CNE-2Z cells
2001
Fas ligand is targeted to secretory lysosomes via a proline-rich domain in its cytoplasmic tail
Blott E, Bossi G, Clark R, Zvelebil M, Griffiths G. Fas ligand is targeted to secretory lysosomes via a proline-rich domain in its cytoplasmic tail. Journal Of Cell Science 2001, 114: 2405-2416. PMID: 11559749, DOI: 10.1242/jcs.114.13.2405.Peer-Reviewed Original ResearchConceptsProline-rich domainSecretory lysosomesPlasma membraneCytoplasmic tailSH3 domain-containing proteinsCell surface receptor FasFas ligandCell surface expression of FasLSH3-domain-containingSurface expression of FasLCell typesPositively charged residuesMis-sortingSorting motifDeletion mutantsExpression of FasLReceptor FasEndogenous FasLInduce apoptosisCharged residuesCell surface expressionLysosomal compartmentFasLLysosomesMotif
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