Matches in SemOpenAlex for { <https://semopenalex.org/work/W2535346982> ?p ?o ?g. }
Showing items 1 to 87 of
87
with 100 items per page.
- W2535346982 endingPage "4920" @default.
- W2535346982 startingPage "4920" @default.
- W2535346982 abstract "Abstract Backgrounds: The long term prognosis of adult B-lineage acute lymphoblastic leukemia (B-ALL) is poor when compared with pediatric B-ALL. The current therapeutic regimen for adult B-ALL often results in refractory and relapsing diseases. Therefore, it is urgently needed to explore novel approaches to treat adult B-ALL. Disulfiram (DS) has been used clinically as a safe anti-alcoholism drug for over 6 decades. Recent studies demonstrated that disulfiram/cooper mixture (DS/Cu) was cytotoxic to multiple solid cancers, but its effects on B-ALL cells are still unclear. Moreover, the molecular mechanism of the cytotoxicity of DS/Cu to tumor cells was poorly defined. In this study, we investigated the effects of DS/Cu on B-ALL cells in vitro and its related cytotoxic mechanism. Results: Firstly, CCK8 assay indicated that DS/Cu markedly inhibited Nalm6 cell proliferation in a dose-dependent manner. Secondly, colony-forming assay showed that DS/Cu also abolished the clonogenicity of Nalm6 cells (P<0.001). Thirdly, FACS analyses revealed that DS/Cu mixture could induce apoptosis of Nalm6 cells, as well as primary B-ALL cells (n=16) in a dose-dependent manner. We additionally analyzed the relationship between clinical characteristics of B-ALL patients, including age, WBC counts, immunophenotype, cytogenetics, risk stratification and Ph chromosome, with the efficacy of DS/Cu on B-ALL cells. The apoptosis isolated from pro-B and cytogenetic abnormality B-ALL pastients was higher. Therefore, our results demonstrated that DS/Cu mixture could induce significant cytotoxicity against B-ALL cells in vitro. To decipher the cytotoxic mechanism of DS/Cu mixture, JC-1 staining was done and the results showed that DS/Cu mixture could significantly reduce the mitochondrial membrane potential in Nalm6 cells (P<0.01) and 7 cases of primary B-ALL cells (P<0.05). Consistently, Western Blot analysis showed that DS/Cu induced B-ALL cell apoptosis by down-regulating the expression of anti-apoptotic protein Bcl2 and Bcl-XL, as well as activating caspase-3 and its substrate PARP. Hence, our results indicated that DS/Cu induced apoptosis of B-ALL cells at least partly through the intrinsic mitochondrial apoptotic pathway. Conclusion: Our results demonstrated that DS/Cu not only significantly inhibit proliferation and clonogenicity, but also induce apoptosis of B-ALL cells in vitro.The mitochondrial apoptotic pathway might be the molecular mechanism of DS/Cu-induced apoptosis of B-ALL cells. Disclosures No relevant conflicts of interest to declare." @default.
- W2535346982 created "2016-10-28" @default.
- W2535346982 creator A5004747587 @default.
- W2535346982 creator A5019873683 @default.
- W2535346982 creator A5028097742 @default.
- W2535346982 creator A5073976864 @default.
- W2535346982 creator A5087837180 @default.
- W2535346982 creator A5091783710 @default.
- W2535346982 date "2015-12-03" @default.
- W2535346982 modified "2023-09-30" @default.
- W2535346982 title "Role of Mitochondrial Apoptotic Pathway in Disulfiram/Copper Mixture-Induced Cell Apoptosis in Human B-Lineage Acute Lymphoblastic Leukemia in Vitro" @default.
- W2535346982 doi "https://doi.org/10.1182/blood.v126.23.4920.4920" @default.
- W2535346982 hasPublicationYear "2015" @default.
- W2535346982 type Work @default.
- W2535346982 sameAs 2535346982 @default.
- W2535346982 citedByCount "1" @default.
- W2535346982 countsByYear W25353469822021 @default.
- W2535346982 crossrefType "journal-article" @default.
- W2535346982 hasAuthorship W2535346982A5004747587 @default.
- W2535346982 hasAuthorship W2535346982A5019873683 @default.
- W2535346982 hasAuthorship W2535346982A5028097742 @default.
- W2535346982 hasAuthorship W2535346982A5073976864 @default.
- W2535346982 hasAuthorship W2535346982A5087837180 @default.
- W2535346982 hasAuthorship W2535346982A5091783710 @default.
- W2535346982 hasConcept C109316439 @default.
- W2535346982 hasConcept C126322002 @default.
- W2535346982 hasConcept C154317977 @default.
- W2535346982 hasConcept C185592680 @default.
- W2535346982 hasConcept C190283241 @default.
- W2535346982 hasConcept C196166836 @default.
- W2535346982 hasConcept C202751555 @default.
- W2535346982 hasConcept C203014093 @default.
- W2535346982 hasConcept C2776694085 @default.
- W2535346982 hasConcept C2778119113 @default.
- W2535346982 hasConcept C2778461978 @default.
- W2535346982 hasConcept C502942594 @default.
- W2535346982 hasConcept C54355233 @default.
- W2535346982 hasConcept C553184892 @default.
- W2535346982 hasConcept C71924100 @default.
- W2535346982 hasConcept C86803240 @default.
- W2535346982 hasConceptScore W2535346982C109316439 @default.
- W2535346982 hasConceptScore W2535346982C126322002 @default.
- W2535346982 hasConceptScore W2535346982C154317977 @default.
- W2535346982 hasConceptScore W2535346982C185592680 @default.
- W2535346982 hasConceptScore W2535346982C190283241 @default.
- W2535346982 hasConceptScore W2535346982C196166836 @default.
- W2535346982 hasConceptScore W2535346982C202751555 @default.
- W2535346982 hasConceptScore W2535346982C203014093 @default.
- W2535346982 hasConceptScore W2535346982C2776694085 @default.
- W2535346982 hasConceptScore W2535346982C2778119113 @default.
- W2535346982 hasConceptScore W2535346982C2778461978 @default.
- W2535346982 hasConceptScore W2535346982C502942594 @default.
- W2535346982 hasConceptScore W2535346982C54355233 @default.
- W2535346982 hasConceptScore W2535346982C553184892 @default.
- W2535346982 hasConceptScore W2535346982C71924100 @default.
- W2535346982 hasConceptScore W2535346982C86803240 @default.
- W2535346982 hasIssue "23" @default.
- W2535346982 hasLocation W25353469821 @default.
- W2535346982 hasOpenAccess W2535346982 @default.
- W2535346982 hasPrimaryLocation W25353469821 @default.
- W2535346982 hasRelatedWork W1544481176 @default.
- W2535346982 hasRelatedWork W1861055009 @default.
- W2535346982 hasRelatedWork W1987594535 @default.
- W2535346982 hasRelatedWork W2119766186 @default.
- W2535346982 hasRelatedWork W2335526988 @default.
- W2535346982 hasRelatedWork W2390772360 @default.
- W2535346982 hasRelatedWork W2523232728 @default.
- W2535346982 hasRelatedWork W2531526805 @default.
- W2535346982 hasRelatedWork W2535054682 @default.
- W2535346982 hasRelatedWork W2559787406 @default.
- W2535346982 hasRelatedWork W2564864293 @default.
- W2535346982 hasRelatedWork W2574114787 @default.
- W2535346982 hasRelatedWork W2623545481 @default.
- W2535346982 hasRelatedWork W2966220900 @default.
- W2535346982 hasRelatedWork W2979694512 @default.
- W2535346982 hasRelatedWork W3029414653 @default.
- W2535346982 hasRelatedWork W3029857048 @default.
- W2535346982 hasRelatedWork W3139795097 @default.
- W2535346982 hasRelatedWork W3141921296 @default.
- W2535346982 hasRelatedWork W3198867227 @default.
- W2535346982 hasVolume "126" @default.
- W2535346982 isParatext "false" @default.
- W2535346982 isRetracted "false" @default.
- W2535346982 magId "2535346982" @default.
- W2535346982 workType "article" @default.