ArticlePloS one2013
EVI1 inhibits apoptosis induced by antileukemic drugs via upregulation of CDKN1A/p21/WAF in human myeloid cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- High expression of myocyte enhancer factor 2C (MEF2C) is associated with adverse-risk features and poor outcome in pediatric acute myeloid leukemia: a report from the Children's Oncology Group.Journal of hematology & oncology · 2015Trial
- MECOM promotes supporting cell proliferation and differentiation in cochlea.Journal of otology · 2022Article
- Evi1 upregulates Fbp1 and supports progression of acute myeloid leukemia through pentose phosphate pathway activation.Cancer science · 2021Article
- MECOM permits pancreatic acinar cell dedifferentiation avoiding cell death under stress conditions.Cell death and differentiation · 2021Article
- Article
- EVI1 promotes epithelial-to-mesenchymal transition, cancer stem cell features and chemo-/radioresistance in nasopharyngeal carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Imbalanced expression of polycistronic miRNA in acute myeloid leukemia.International journal of hematology · 2017Article
- Article
- Nucleotide-binding oligomerization domain 1 acts in concert with the cholecystokinin receptor agonist, cerulein, to induce IL-33-dependent chronic pancreatitis.Mucosal immunology · 2016Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
- p21(WAF1) modulates drug-induced apoptosis and cell cycle arrest in B-cell precursor acute lymphoblastic leukemia.Cell cycle (Georgetown, Tex.) · 2015Article
- Targeted next-generation sequencing reveals high frequency of mutations in epigenetic regulators across treatment-naïve patient melanomas.Clinical epigenetics · 2015Article
- The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.Cell cycle (Georgetown, Tex.) · 2014Article
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Authors and funding
18 authors.
Funding
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Abstract
Overexpression of ecotropic viral integration site 1 (EVI1) is associated with aggressive disease in acute myeloid leukemia (AML). Despite of its clinical importance, little is known about the mechanism through which EVI1 confers resistance to antileukemic drugs. Here, we show that a human myeloid cell line constitutively overexpressing EVI1 after infection with a retroviral vector (U937_EVI1) was partially resistant to etoposide and daunorubicin as compared to empty vector infected control cells (U937_vec). Similarly, inducible expression of EVI1 in HL-60 cells decreased their sensitivity to daunorubicin. Gene expression microarray analyses of U937_EVI1 and U937_vec cells cultured in the absence or presence of etoposide showed that 77 and 419 genes were regulated by EVI1 and etoposide, respectively. Notably, mRNA levels of 26 of these genes were altered by both stimuli, indicating that EVI1 regulated genes were strongly enriched among etoposide regulated genes and vice versa. One of the genes that were induced by both EVI1 and etoposide was CDKN1A/p21/WAF, which in addition to its function as a cell cycle regulator plays an important role in conferring chemotherapy resistance in various tumor types. Indeed, overexpression of CDKN1A in U937 cells mimicked the phenotype of EVI1 overexpression, similarly conferring partial resistance to antileukemic drugs.
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