2000
The antiangiogenic agent TNP-470 requires p53 and p21CIP/WAF for endothelial cell growth arrest
Yeh J, Mohan R, Crews C. The antiangiogenic agent TNP-470 requires p53 and p21CIP/WAF for endothelial cell growth arrest. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 12782-12787. PMID: 11070090, PMCID: PMC18841, DOI: 10.1073/pnas.97.23.12782.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiogenesis InhibitorsAnimalsCell CycleCell DivisionCells, CulturedCorneal NeovascularizationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsCyclohexanesEndothelium, VascularGene ExpressionHumansMiceMice, KnockoutNuclear ProteinsO-(Chloroacetylcarbamoyl)fumagillolProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2SesquiterpenesTumor Suppressor Protein p53ConceptsTNP-470Endothelial cellsAntiangiogenic agent TNP-470Subsequent growth arrestGrowth arrestCyclin-dependent kinase inhibitorAntiangiogenic strategiesPrimary endothelial cellsEndothelial cell growth arrestP21CIP/WAFEndothelial cell cycleCell growth arrestKinase inhibitorsAntiangiogenic activityCell cycle regulatorsAngiogenesis assayCytostatic activityP53 activationMiceCritical cell cycle regulatorsCycle regulatorsUnique mechanismAdult fibroblastsCell-type specificityArrest
1999
Eponemycin exerts its antitumor effect through the inhibition of proteasome function.
Meng L, Kwok BH, Sin N, Crews CM. Eponemycin exerts its antitumor effect through the inhibition of proteasome function. Cancer Research 1999, 59: 2798-801. PMID: 10383134.Peer-Reviewed Original ResearchConceptsProteasome inhibitionCyclin-dependent kinase inhibitorNovel chemotherapeutic strategiesPharmacological interventionsAntitumor effectsPossible cancer therapySubunits LMP2Chemotherapeutic strategiesKinase inhibitorsCellular morphological changesCell cycle progressionCancer therapyCycle progressionInhibitionProteasome functionMorphological changesKey regulatory proteinsProteasomal subunitsTherapy