Unknown,Transcriptomics,Genomics,Proteomics

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SOX7-enforced expression promotes the expansion of adult blood progenitors and blocks B cell development

ABSTRACT: Here we use a microarray approach to define at the molecular level the consequences of SOX7-mediated effect on B lymphopoiesis and progenitor proliferation. Transcriptome profiling analysis was performed on two subpopulations expressing low and high level of SOX7::GFP. Bone marrow cells extracted from iSox7 transgenic mice were treated with and without dox in duplicate

ORGANISM(S): Mus musculus

SUBMITTER: Valerie Kouskoff

PROVIDER: E-GEOD-65552 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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SOX7-enforced expression promotes the expansion of adult blood progenitors and blocks B-cell development.

Cuvertino Sara S Lacaud Georges G Kouskoff Valerie V

Open biology 20160701 7

During embryogenesis, the three SOXF transcription factors, SOX7, SOX17 and SOX18, regulate the specification of the cardiovascular system and are also involved in the development of haematopoiesis. The ectopic expression of SOX17 in both embryonic and adult blood cells enhances self-renewal. Likewise, the enforced expression of SOX7 during embryonic development promotes the proliferation of early blood progenitors and blocks lineage commitment. However, whether SOX7 expression can also affect t ...[more]

PMID: 27411892

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Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy characterized by infiltration of the bone marrow and other sites with transformed T cell progenitors. The role of tissue microenvironments in the pathogenesis of T-ALL or any other type of acute leukemia is little understood. In delineating interactions between T-ALL cells and their environment, we initially found that T-ALL cells express high surface levels of the chemokine receptor CXCR4. Intravital imaging of an intact tibia revealed T-ALL cells in direct contact with bone marrow stromal cells producing the CXCR4 ligand, CXCL12. Genetic targeting of CXCR4 on T-ALL cells resulted in a marked reduction of leukemia burden and prolonged disease remission, and disruption of the CXCL12/CXCR4 axis using small molecule inhibitors prevented T-ALL progression in a primary xenograft model. Finally, we were able to show that CXCR4 inhibition significantly decreased expression of Myc and its target genes. Myc expression is a key regulator of T-ALL leukemia initiating cell (LIC) activity, suggesting that CXCR4 inhibition can suppress LIC activity by silencing the Myc response in T-ALL cells. Our data suggest that targeting of CXCL12/CXCR4 signaling could be a powerful new tool for combating T-ALL, a disease with no current targeted therapies. Mouse T-ALL cells were treated ex vivo with Cxcr4 inhibitor AMD3100 or vehicle control. Additionally, mouse T-ALL primary tumors were isolated from control (Cxcr4+/+) or knockout (Cxcr4-/-) animals. Total RNA was extracted from samples using the RNeasy Plus Mini Kit (Qiagen). Samples were then subject to PolyA selection using oligo-dT beads (Life Technologies, Carlsbad, CA) according to the manufacturer's instructions. The resulting RNA samples were then used as input for library construction using the dUTP method as described by Parkhomchuck et al., 2009. RNA libraries were then sequenced on the Illumina HiSeq 2500 using 50bp single-end reads.

Dataset Information

SOX7-enforced expression promotes the expansion of adult blood progenitors and blocks B cell development

Publications

SOX7-enforced expression promotes the expansion of adult blood progenitors and blocks B-cell development.

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