Amide and ester derivatives of chlorido[4-carboxy-1,2-disalicylideneaminobenzene]iron(iii) as necroptosis and ferroptosis inducers

2020 ◽  
Vol 49 (20) ◽  
pp. 6842-6853 ◽  
Author(s):  
Daniel Baecker ◽  
Benjamin N. Ma ◽  
Jessica Sagasser ◽  
Lukas Schultz ◽  
Carina Hörschläger ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Acute Myeloid Leukemia Cell ◽  
Leukemia Cell Line ◽  
Derivatives Of ◽  
Acute Myeloid ◽  
Myeloid Leukemia Cell

Amide and ester derivatives of chlorido[4-carboxy-1,2-disalicylideneaminobenzene]iron(iii) were synthesized and characterized as necroptosis and ferroptosis inducers using the acute myeloid leukemia cell line HL-60.

Abstract 277: Genetic re-programming of the acute myeloid leukemia cell line HL-60

2011 ◽  
Author(s):  
Michael Roberts ◽  
David Bittner ◽  
Sarah Brnich ◽  
Bryan Conner ◽  
Carla Cox ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Acute Myeloid Leukemia Cell ◽  
Leukemia Cell Line ◽  
Acute Myeloid ◽  
Myeloid Leukemia Cell

GEFITINIB EFFECTS IN A NPM1-MUTATED ACUTE MYELOID LEUKEMIA CELL LINE

2020 ◽  
Vol 129 (1) ◽  
pp. e159
Author(s):  
NAYARA FERREIRA DE ABREU ◽  
CAMILA CRISTINA OLIVEIRA MENEZES BONALDO ◽  
PATRICIA VIANNA BONINI PALMA ◽  
EDUARDO MAGALHÃES REGO ◽  
LUCIANA YAMAMOTO DE ALMEIDA
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Acute Myeloid Leukemia Cell ◽  
Leukemia Cell Line ◽  
Acute Myeloid ◽  
Myeloid Leukemia Cell

DNMT3A R882H mutation in acute myeloid leukemia cell line SET-2

2020 ◽  
Vol 88 ◽  
pp. 106270
Author(s):  
Hilmar Quentmeier ◽  
Claudia Pommerenke ◽  
Wilhelm G. Dirks ◽  
Silke Fähnrich ◽  
Vivien Hauer ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Acute Myeloid Leukemia Cell ◽  
Leukemia Cell Line ◽  
Acute Myeloid ◽  
Myeloid Leukemia Cell

Drug-sensitivity of resistant acute myeloid leukemia cell line to Doxorubicin is enhanced by Triptolide through down-regulation of HIF-1α and Nrf2

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4921-4921
Author(s):  
Bing Xu ◽  
Feili Chen ◽  
Yuejian Liu ◽  
Shiyun Wang ◽  
Rongwei Li ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Drug Sensitivity ◽  
Target Genes ◽  
Leukemia Cell ◽  
Acute Myeloid Leukemia Cell ◽  
Leukemia Cell Line ◽  
Acute Myeloid ◽  
Myeloid Leukemia Cell

Abstract Background Relapse and treatment-related complication have been the hurdle for the cure of acute myeloid leukemia patients. Finding a new drug-sensitizer could significantly prolong the survival time of patients. Triptolide (TPL) has been shown to enhance the drug-sensitivity of a variety of cancer cells when used in a low-concentration. HL60/DOX is a kind of acute myeloid leukemia cell line which is resistant to a commonly used drug Doxorubicin. This kind of cell line is widely used in the study of drug-sensitization. Aim This study aims to investigate whether low-dose TPL could enhance the drug-sensitivity of resistant acute myeloid leukemia cell line HL60/DOX to Doxorubicin and related mechanism. Method HL60/DOX cells were subjected to different treatments and thereafter MTT assay, flow cytometry and Western blot or RT-PCR were used to determine IC50, apoptotic status and expression of Nrf2, HIF-1α and their target genes. Results HL60/DOX cells were exposed to increasing concentrations of Doxorubicin with TPL at a constant IC20 concentration (14nM) for 48h. In comparison with anticancer agent alone, TPL enhanced the cytotoxicity of Doxorubicin (IC50:14.36±2.23 vs. 7.9±0.33μM, 1.82 fold; P=0.008) to HL60/DOX. Results of combination index showed that TPL and anti-cancer agents had synergistic effects when fraction affected was below 60%. Flow cytometry analysis also showed that apoptoticratio of cells treated by Doxorubicin together with TPL was significantly increased compared to cell streated by Doxorubicin alone (19.55±1.70%vs. 72.62±4.83%, P<0.01). Next, we explored the underlying mechanism. Hypoxia-inducible factor- 1α (HIF-1α) is the major mediator of hypoxic responses in malignant cells. High expression of it is correlated with bad clinical outcome in patients. It is also important for the survival of leukemia stem cells which are responsible for relapse. Nrf2 is an important protective factor which is correlated with chemo-resistance in cancer cells. When combined with TPL, Doxorubicin down-regulates Nrf2 and HIF-1α expression at protein and mRNA levels. Down-stream genes of Nrf2 e.g NQO1, GSR and HO-1 as well as target genes of HIF-1α e.g BNIP3, VEGF and CAIX are also down-regulated at mRNA level. Conclusion Inconclusion, our study demonstrates that TPL could enhance drug-sensitivity of HL60/DOX in vitro through down-regulation of Nrf2 and HIF-1α, providing the experimental base for further study. Disclosures: No relevant conflicts of interest to declare.

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