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MiRNA profiling of the MV4-11 cell line treated with trabectidin or azacitidin

ABSTRACT: In order to study the effects of trabectedin in chronic myelomonocytic leukemia and in juvenile myelomonocytic leukemia, we performed whole genome transcriptional profiling of a model cell line treated under either the reference drug for CMML / JMML (Azacitidine) or trabectedin.

ORGANISM(S): Homo sapiens

SUBMITTER: Luca Beltrame

PROVIDER: E-MTAB-2979 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional profiling of the MV4-11 cell line treated with trabectidin or azacitidin

Project description:In order to study the effects of trabectedin in chronic myelomonocytic leukemia and in juvenile myelomonocytic leukemia, we performed whole genome transcriptional profiling of a model cell line treated under either the reference drug for CMML / JMML (Azacitidine) or trabectedin.

2016-12-14 | E-MTAB-2978 | biostudies-arrayexpress

Whole transcriptome profiling by microarray of monocytes stimulated with LPS and treated with trabectedin, lurbinectedin or doxorubicin

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Whole genome transcription profiling of the JN-DSCRT1 cell line treated with Trabectedin

Project description:The purpose of experiments consisted in studying the mode of action of Trabectedin in Desmoplastic Small Round Cell Tumor (DSRCT). In order to investigate the effects of Trabectedin in the expression of EWS-WT1 target genes in relation to the drug growth inhibitory effect, the JN-DSCRT-1 cell line was treated for 1 hour with 5 nM of Trabectedin. Samples were collected at 6, 12 and 24 hours after drug washout. Three biological replicates were used for each time point.

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Project description:Juvenile myelomonocytic leukemia (JMML) is caused by constitutively activated RAS signalling and is characterized by increased proliferation and predominant myelomonocytic differentiation of hematopoietic cells. Using Mx-Cre;PTPN11D61Y mice, which reflect human JMML, we show that RAS pathway activation affects apoptosis signalling through cell type-dependent regulation of BCL-2 family members. Apoptosis resistance observed in monocytes and granulocytes was mediated by overexpression of the anti-apoptotic and down-regulation of the pro-apoptotic members of the BCL-2 family. Two anti-apoptotic proteins, BCL-XL and MCL-1, were directly regulated by the oncogenic RAS signalling but in addition were influenced by microenvironmental signals. While BCL-XL and BCL-2 were required for the survival of monocytes, MCL-1 was essential for neutrophils. Interestingly, stem and progenitor cells expressing the oncogenic PTPN11 mutant did not display any increased apoptosis resistance. BCL-XL inhibition was the most effective in killing myeloid cells in vitro but was not sufficient to completely resolve myeloproliferation in vivo.

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Long-term proliferation of immature hypoxia-dependent JMML cells supported by a 3D in vitro system

Project description:Juvenile myelomonocytic leukemia (JMML) is a rare stem cell disorder occurring in early childhood and characterized by RAS pathway hyperactivation in 95% of patients. JMML is identified by a hyperproliferation of granulocyte and monocyte, and little is known about the heterogeneous nature of leukemia initiating cells as well as the cellular hierarchy of the JMML bone marrow (BM). In this study, we reported the generation and characterization of a novel patient-derived 3D in vitro JMML model (pd-JAO) sustaining long-term proliferation of JMML cells with stem cell features and patient specific hallmarks. JMML cells brewed in the 3D model under different microenvironmental conditions acquired a proliferative and survival advantage when placed at low oxygen tensions. Transcriptomic and microscopic analysis revealed the activation of specific metabolic energy pathways and the inactivation of processes leading to cell death. Furthermore, we demonstrated pd-JAO derived cells’ migratory, propagation and self-renewal capacities both in in vitro and in vivo mouse model. Our study contributed to the development of a robust JMML 3D in vitro model to study and comprehend the impact of microenvironment stimuli on JMML disease and the molecular mechanisms regulating JMML initiating and propagating cells. Pd-JAO may become a promising model for compound tests focusing on new therapeutic intervention aiming to eradicate JMML progenitors and control JMML disease. We defined a 3D in vitro model that under hypoxic conditions is able to sustain long-term propagation of JMML-patients cells with specific hallmarks. Different oxygen level enviroment drive specific metabolic switch that prompts JMML cells to self-renewal.

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