Comparison of K562 Chronic Myeloid Leukemia cells with resistant counterparts
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PROVIDER: PRJNA1269965 | ENA |
REPOSITORIES: ENA
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Project description:We analyzed differential gene expression by comparing K562-R (drug-resistant) and K562 (wild-type) cells. This supplementary analysis provides valuable context by revealing transcriptional changes associated with acquired resistance, highlighting biological processes that may contribute to the drug-resistant phenotype in chronic myeloid leukemia (CML).
2025-07-17 | GSE298575 | GEO
Project description:The aim of the analysis is to study the relationship between tyrosine kinase inhibitor (TKI) resistance mechanism and phenotypic plasticity in the TKI-resistant and parental chronic myeloid leukemia K562 cell lines, in the presence and absence of imatinib. Results provide insight into the molecular mechanisms underlying the acquisition of cancer cell plasticity.
2020-04-14 | GSE120932 | GEO
Project description:K562 cells, a myeloid leukemia cells line, were engineered to express a tamoxifen inducible dominant negative Myb (MERT). K562-MERT cells were cultured for 3 days in the absence and presence of 1 uM tamoxifen. The RNA was then extracted from the untreated and tamoxifen treated K562-MERT cells and submitted to Incyte Genomics for poly(A) RNA selection, probe preparation, hybridization of the labeled cDNA to the micorarray chip (Incyte Genomics) and data analysis.
2004-06-30 | E-MEXP-91 | biostudies-arrayexpress
Project description:Whole-genome gene expression comparison of the chronic myeloid leukemia cell line K562 and its tyrosine kinase inhibitor resistant subclone K562-IR.
| PRJNA495056 | ENA
Project description:Using a microarray-based miRNA profiling, we found in a model of chronic myeloid leukemia (CML) that the activity of the oncoprotein BCR-ABL1 regulates the expression of miR-21, a "onco-microRNA" known to be overexpressed in numerous cancers. This relies on the phosphorylation status of STAT5, a transcription factor known to be activated by the kinase activity of BCR-ABL1. Mir-21 regulates the expression of PDCD4 (programmed cell death protein 4), a tumor suppressor identified here through a proteomics approach The microRNA repertoire of K562 cells having been either not treated (n=3) or treated (n=3) with the tyrosine kinase inhibitor Imatinib (1microM, 24h) was studied using Agilent microRNA V2 microarrays
2016-09-01 | E-GEOD-78037 | biostudies-arrayexpress
Project description:Inhibition of deregulated protein kinases by small molecule drugs has evolved into a major therapeutic strategy for the treatment of human malignancies. Imatinib mesylate has emerged as the leading compound to treat chronic myeloid leukemia (CML), through its inhibition of Bcr- Abl tyrosine kinases, and other cancers. However, resistance to imatinib develops frequently, particularly in late-stage disease and has necessitated the development of new BCR-ABL inhibitors. The synthesis of a new series of phenylaminopyrimidines, structurally related to imatinib showed large interest since the introduction of the nilotibin. To identify the cellular pathways affected by new synthesized compounds, we applied mass spectrometry together with stable isotope labeling by amino acids in cell culture (SILAC) for the comparative study of protein expression in K562 cells that were untreated or treated with imatinib and imatinib derivates. Further, the global proteome of the K562 cells treated with imatinib were quantitatively compared with the cells treated with the new compounds. This study enriched our knowledge about direct cellular targets of kinase selective drugs. Further the results offered important new knowledge for gaining insights into the structural effects of action of the new compounds. Samples were analyzed on a longer column (30cm) and a longer gradient (180min). Raw data files were processed with Mascot distiller 2.3. The mgf files were searched with Mascot daemon 2.3. The quantification was also done by Mascot Distiller. All data was stored in ms_lims. The manual validation of false peptide ratios was done with Rover (part of ms_lims). Fixed modifications: none. Variable modifications: acetylation of peptide N-terminus, pyroglutamate formation of N-terminal glutamine, methionine oxidation. Enzyme: trypsine with one missed cleavage allowed. Precursor mass tolerance: 10 ppm. Peptide fragment mass tolerance: 0.5 Da Quantitation method: SILAC arginine and lysine +6 Da. Overview of the 17 different analyses: B SK23 vs DMSO C Y22 vs DMSO D SK20 vs DMSO E Y18 vs DMSO I SK20 vs DMSO K Y18 vs DMSO O Y22 vs DMSO R Imatinib vs Water Z Imatinib vs Water J SK20 vs Imatinib M SK23 vs Imatinib N Y22 vs Imatinib P SK23 vs Imatinib Q Y18 vs Imatinib S Y22 vs Imatinib T SK20 vs Imatinib Y Y18 vs Imatinib
2014-06-30 | PXD000216 | Pride
Project description:Chronic and acute myeloid leukemia (CML/AML) evade immune surveillance and induce immunosuppression, largely by upregulating Foxp3+ regulatory T cells (Treg). However, mechanisms that drive Treg in myeloid leukemias are largely unknown. Here, we show that leukemic (CML- and AML-derived) extracellular vesicles (EVs) drive human Treg, by de novo induction of Treg and by upregulating suppressive phenotype and activity of Treg. Rab27a-mediated EVs secretion contributed to Treg expansion, activity, and leukemic engraftment in vivo in a mouse model of CML-like disease. Leukemic EVs downregulated mTOR-S6 and upregulated STAT5 signaling in T cells, to upregulate Foxp3 and Treg activity, as well as evoked significant transcriptomic changes in Treg. By using high resolution 23-color spectral flow cytometry we identified 2 distinct, highly suppressive subsets of Treg expanded by leukemic EVs, characterized by elevated expression of tumor Treg markers CCR8, CCR4, TIGIT, CD39, CD30, TNFR2 and IL21R. Finally, we identified 4 1BBL/TNFSF9 protein in leukemic EVs. Deficiency of 4-1BBL in leukemic cells and EVs resulted in lower expression of CD30, TNFR2 and LAG-3 on Treg and thus weaker effector phenotype. Collectively, our data pinpoint leukemic extracellular vesicles as a significant factor that drives regulatory T cells and immunosuppression in myeloid leukemias. Our results suggest that targeting of Rab27a and EVs secretion may be a viable therapeutic option in myeloid leukemias, whereas detection of 4 1BBL containing EVs could be used as an early biomarker of immunosuppression and leukemia development/relapse
2022-02-16 | PXD027240 | Pride
Project description:To explore the mechanisim and signaling pathway of hypomethylating agent decitabine in reversing P-glycoprotein(P-gp) induced multidrug resistance, we used adriamycin to treat drug sensitive human chronic myeloid leukemia K562 cells(KS) and successfully induced multidrug-resistant K562/ADR (KA) cells that higher expression of drug efflux pump P-gp. Gene expression profile was used to analysis the difference gene expression before and after treated with decitabine in both KS and KA cells.
2018-03-01 | GSE93942 | GEO
Project description:UnlabelledBackgroundCancer is one of the most prominent human diseases which has enthused scientific and commercial interest in the discovery of newer anticancer agents from natural sources. Here we demonstrated the anticancer activity of ethanolic extract of aerial parts of Pupalia lappacea (L) Juss (Amaranthaceae) (EAPL) on Chronic Myeloid Leukemia K562 cells.MethodsAntiproliferative activity of EAPL was determined by MTT assay using carvacrol as a positive control. Induction of apoptosis was studied by annexin V, mitochondrial membrane potential, caspase activation and cell cycle analysis using flow cytometer and modulation in protein levels of p53, PCNA, Bax and Bcl2 ratio, cytochrome c and cleavage of PARP were studied by Western blot analysis. The standardization of the extract was performed through reverse phase-HPLC using Rutin as biomarker.ResultsThe results showed dose dependent decrease in growth of K562 cells with an IC50 of 40 ± 0.01 μg/ml by EAPL. Induction of apoptosis by EAPL was dose dependent with the activation of p53, inhibition of PCNA, decrease in Bcl2/Bax ratio, decrease in the mitochondrial membrane potential resulting in release of cytochrome c, activation of multicaspase and cleavage of PARP. Further HPLC standardization of EAPL showed presence 0.024% of Rutin.ConclusionPresent study significantly demonstrates anticancer activity of EAPL on Chronic Myeloid Leukemia (K562) cells which can lead to potential therapeutic agent in treating cancer. Rutin, a known anti cancer compound is being reported and quantified for the first time from EAPL.
| S-EPMC3559012 | biostudies-literature
Project description:Medium-dependent gene-expression profiling of the human K562 chronic myeloid leukemia cell line
| PRJNA691568 | ENA