ArticleOncogene2007
Apoptosis and erythroid differentiation triggered by Bcr-Abl inhibitors in CML cell lines are fully distinguishable processes that exhibit different sensitivity to caspase inhibition.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 53 citations in OpenAlex.
- Cabozantinib promotes erythroid differentiation in K562 erythroleukemia cells through global changes in gene expression and JNK activation.Cancer gene therapy · 2022Article
- Perturbation of p38α MAPK as a Novel Strategy to Effectively Sensitize Chronic Myeloid Leukemia Cells to Therapeutic BCR-ABL Inhibitors.International journal of molecular sciences · 2021Article
- Pharmacologic targeting of the P-TEFb complex as a therapeutic strategy for chronic myeloid leukemia.Cell communication and signaling : CCS · 2021Article
- A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway.Molecular therapy oncolytics · 2020Article
- Arsenic sulfide nanoformulation induces erythroid differentiation in chronic myeloid leukemia cells through degradation of BCR-ABL.International journal of nanomedicine · 2019Article
- Montelukast enhances cytocidal effects of carfilzomib in multiple myeloma by inhibiting mTOR pathway.Cancer biology & therapy · 2019Article
- Metabolic Reprogramming During Multidrug Resistance in Leukemias.Frontiers in oncology · 2018Article
- Combined MEK and Pi3'-kinase inhibition reveals synergy in targeting thyroid cancer in vitro and in vivo.Oncotarget · 2017Article
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- p38MAPK and Chemotherapy: We Always Need to Hear Both Sides of the Story.Frontiers in cell and developmental biology · 2016Review
- All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.Oncotarget · 2012Article
- The caspase 6 derived N-terminal fragment of DJ-1 promotes apoptosis via increased ROS production.Cell death and differentiation · 2012Article
- BCL2L10 is a predictive factor for resistance to azacitidine in MDS and AML patients.Oncotarget · 2012Article
- MicroRNA-193a represses c-kit expression and functions as a methylation-silenced tumor suppressor in acute myeloid leukemia.Oncogene · 2011Article
- Leukemic cell xenograft in zebrafish embryo for investigating drug efficacy.Haematologica · 2011Article
- A new hydroxylated nonaprenylhydroquinone from the Mediterranean marine sponge Sarcotragus spinosulus.Marine drugs · 2011Article
- Targeting lysosomes to eradicate imatinib-resistant chronic myelogenous leukemia cells.Leukemia · 2010Article
- Article
- Acadesine kills chronic myelogenous leukemia (CML) cells through PKC-dependent induction of autophagic cell death.PloS one · 2009Article
- Inhibition of imatinib-mediated apoptosis by the caspase-cleaved form of the tyrosine kinase Lyn in chronic myelogenous leukemia cells.Leukemia · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib targets the Bcr-Abl oncogene that causes chronic myelogenous leukemia (CML) in humans. Recently, we demonstrated that besides triggering apoptosis in K562 cells, imatinib also mediated their erythroid differentiation. Although both events appear to proceed concomitantly, it is not known at present whether or not imatinib-induced apoptosis and differentiation are interdependent processes. Hence, we investigated the requirements for Bcr-Abl inhibitor-mediated apoptosis and erythroid differentiation in several established and engineered CML cell lines. Imatinib triggered apoptosis and erythroid differentiation of different CML cell lines, but only apoptosis exhibited sensitivity to ZVAD-fmk inhibition. Conversely, the p38 mitogen-activated protein (MAP) kinase inhibitor, SB202190, significantly slowed down erythroid differentiation without affecting caspase activation. Furthermore, imatinib and PD166326, another Bcr-Abl inhibitory molecule, triggered erythroid differentiation of K562 cell clones, nevertheless resistant to Bcr-Abl inhibitor-induced apoptosis. Finally, short hairpin RNA inhibitor (shRNAi) silencing of caspase 3 efficiently inhibited caspase activity but had no effect on erythroid differentiation, whereas silencing of Bcr-Abl mimicked imatinib or PD166326 treatment, leading to increased apoptosis and erythroid differentiation of K562 cells. Taken together, our findings not only demonstrate that Bcr-Abl inhibitor-mediated apoptosis and differentiation are fully distinguishable events, but also that caspases are dispensable for erythroid differentiation of established CML cell lines.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.