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Functional roles of STIM1::MXD3 in K562 myeloid leukemic cells and its impact on MYC transcriptional control [K562_STIM1-MXD3]

ABSTRACT: Functional roles of STIM1::MXD3 in K562 myeloid leukemic cells and its impact on MYC transcriptional control [K562_STIM1-MXD3]

PROVIDER: PRJNA923604 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23073300_1.fastq.gz	Fastqsanger.gz
	SRR23073300_2.fastq.gz	Fastqsanger.gz
	SRR23073301_1.fastq.gz	Fastqsanger.gz
	SRR23073301_2.fastq.gz	Fastqsanger.gz
	SRR23073302_1.fastq.gz	Fastqsanger.gz

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Functional roles of STIM1::MXD3 in K562 myeloid leukemic cells and its impact on MYC transcriptional control [K562_STIM1-MXD3]

Project description:To investigate the functional significance of STIM1::MXD3, we overexpressed the fusion gene in K562 myeloid leukemia cells and analysed global gene expression changes using RNA-seq.

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STIM1 and STIM2 mediate cancer-induced inflammation in T cell acute lymphoblastic leukemia

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy of T cell progenitors that in most patients is associated with activating mutations in the NOTCH1 pathway. Recent reports have indicated a link between Ca2+ homeostasis in the endoplasmic reticulum (ER), the regulation of NOTCH1 signaling and T-ALL. Here we investigated the role of store-operated Ca2+ entry (SOCE) in T-ALL. SOCE is a Ca2+ influx pathway that is mediated by the plasma membrane Ca2+ channel ORAI1 and its activators STIM1 and STIM2. Deletion of STIM1 and STIM2 in leukemic cells abolished SOCE and significantly prolonged the survival of mice in a NOTCH1-driven model of T-ALL. The survival advantage was unrelated to leukemia development and leukemic cell burden, but was associated with the SOCE-dependent ability of malignant T lymphoblasts to cause inflammation in leukemia-infiltrated organs. Mice with wildtype T-ALL showed a severe necroinflammatory response in their bone marrow, which was absent in mice with Stim1/2-/- leukemia. Several signaling pathways previously linked to cancer-induced inflammation were downregulated in Stim1/2-/- leukemic cells, likely accounting for less aggressive leukemia progression and prolonged survival of mice. Our study shows that T-ALL is associated with inflammation of leukemia-infiltrated organs and that SOCE controls the proinflammatory effects of leukemic T lymphoblasts.

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2019-06-14 | PXD009686 | Pride

CRISPRi RNA-seq from K562 (ENCSR104JMN)

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