Project description:AMPK activation by GSK621 induces cell death in acute myeloid leukemia. Surprisingly, we found that mTORC1 inhibition with rapamycin protects cells against GSK621-induced cytotoxicity. A genome-wide gene expression assay was performed to understand the molecular basis of this phenotype.
Project description:Development and evaluation of an autosampler for integrating nanoPOTS with LC-MS. Includes proteomic data from nanoPOTS-based sample preparation, including diluted peptides of Shewanella oneidensis MR-1, single cultured MCF10A cells, and single cells from three Acute Myeloid Leukemia (AML) cell lines (MOLM-14, K562, and CMK). Data was searched with MaxQuant.
Project description:The human acute myeloid leukemia cell lines MOLM-14 and THP-1 were silenced for MUC1 expression by lentiviral transduction of MUC1 specific shRNA or scrambled control. RNA was extracted and NanoString array for microRNAs was performed.
Project description:MOLM-13 acute myeloid leukemia cells were treated with 3 µM FIDAS-5 methionine S-adenosyltransferase 2A (MAT2A) inhibitor or 0.1% DMSO as control for 48 hours
Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cultured cells. Five cell lines (MOLM-13, SKM-1, F-36P, SKK-1 and OHN-GM) derived from myelodysplastic syndrome patients after progression to acute myeloid leukemia have been studied by flow cytometry, conventional cytogenetics and whole genome single nucleotide polymorphism microarrays, in order to deeply characterize.
Project description:MOLM-13 acute myeloid leukemia cells were treated with 7 µM 5-Azacytidine (Cayman Chemical 11164), or 450 nM CB-5083 (Cayman Chemical 19311), or in combination, or 0.1% DMSO as control. Treatments were conducted for 48 hours.
Project description:Azacytidine (AzaC) and decitabine (AzadC) are cytosine analogs that covalently trap DNA methyltransferases, which place the important epigenetic mark 5-methyl-2’-deoxycytidine by methylating 2’-deoxycytidine (dC) at the C5 position. AzaC and AzadC are used in the clinic as antimetabolites to treat myelodysplastic syndrome and acute myeloid leukemia and are explored against other types of cancer. Although their principal mechanism of action is known, the downstream effects of AzaC and AzadC treatment are not well understood and the cellular prerequisites that determine sensitivity towards AzaC and AzadC remain elusive. Here, we investigated the effects and phenotype of AzaC and AzadC exposure on the acute myeloid leukemia cell line MOLM-13. We found that while AzaC and AzadC share many effects on the cellular level, including decreased global DNA methylation, increased formation of DNA double strand breaks, transcriptional downregulation of important oncogenes and similar changes on the proteome level, AzaC failed in contrast to AzadC to induce apoptosis in MOLM-13. The only cellular marker that correlated with this clear phenotypical outcome was the level of hydroxy-methyl-dC, an additional epigenetic mark that is placed by TET enzymes and repressed in cancer cells. Whereas AzadC increased hmdC substantially in MOLM-13, AzaC treatment did not result in any increase at all. This suggests that hmdC levels in cancer cells should be monitored as a response towards AzaC and AzadC and considered as a biomarker to judge whether AzaC or AzadC lead to cell death in leukemic cells.
Project description:The objective of the sudy is to evalute the role of mTORC1 signalling in the regulation of the metabolism of MOLM-14 cells. We used microarrays to investigate gene expression in MOLM-14 cells after down-regulation of mTORC1 signalling by rapamycin.
Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in leukemia cell line MOLM-13 cells and performed RNA-seq experiments to profile transcriptional changes upon FIS1 depletion.
