WT and Mk2/3 KO MEFs response to etoposide
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Jorge Boucas
PROVIDER: E-GEOD-67266 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Primary mouse embryonic fibroblasts (MEFs) from wt and MK2/3 KO mice were treated with 20µM etoposide.
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Project description: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. Rommer A, Steinmetz B, Herbst F, Hackl H, Heffeter P, Heilos D, Filipits M, Steinleitner K, Hemmati S, Herbacek I, Schwarzinger I, Hartl K, Rondou P, Glimm H, Karakaya K, Krämer A, Berger W, and Wieser R: EVI1 Inhibits Apoptosis Induced by Antileukemic Drugs via Upregulation of CDKN1A/p21/WAF in Human Myeloid Cells. PLoS One 8(2):e56308 (2013). doi: 10.1371/journal.pone.0056308. U937 cells transduced with an EVI1 expression vector or empty vector as control were treated or not with 400 nM etoposide for 48h. 2 biological replicate experiments were performed.
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Project description:We reported a direct phosphorylation of the Ser547 of the RelA/p65 subunit of NF-kB by ATM kinase. A comparative transcriptomic analyse with HEK293 cells expressing exclusively HA-p65wt or a non-phosphorylable mutant HA-p65S547A was conducted to identify the genes regulated by this phosphorylation after an Etoposide treatment. HEK293 cells expressing exclusively HA-p65wt or HA-p65S547A were treated during four or eight hours with Etoposide or left untreated. This was performed three times to obtain independent triplicates for the microarray expermiment.
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Project description:The second leading cause of cancer death for women in the U.S. is breast cancer, moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or M-bM-^@M-^XresistomeM-bM-^@M-^Y of etoposide resitant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. RNA from etoposide-resistant MCF7 (MCF7VP) cell lines were hybridized to Affymetrix microarrays.
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