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Description
This protocol explains the process of how we collected MYCN, MYC, and Histone ChIP-Seq data, as well as ATAC-Seq data for neuroblastoma cell lines. This protocol is comprised of three sections: Cell Growth and Expansion for care of neuroblastoma cell lines, ChIP-Seq protocol, and ATAC-Seq Protocol. Table 1, within the document, outlines which data was collected for each cell line.
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ATAC-Seq of neuroblastoma cell lines.
Dataset
Homo Sapiens
Accession Code
GSE138293
Description
ATAC-Seq of neuroblastoma cell lines.
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MYCN and MYC ChIP-Seq profiling in neuroblastoma cell lines
Dataset
Homo Sapiens
Accession Code
GSE138295
Description
MYCN and MYC profiling in neuroblastoma cell lines
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Histone ChIP-Seq of neuroblastoma cell lines
Dataset
Homo Sapiens
Accession Code
GSE138314
Description
Histone ChIP-Seq of neuroblastoma cell lines
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Transcriptomic Profiling of 39 Neuroblastoma Cell Lines
Dataset
Homo Sapiens
Accession Code
GSE89413
Description
Neuroblastoma cell lines are an important and cost-effective model used to study oncogenic drivers of the disease. While many of these cell lines have been previously characterized with SNP, methylation, and/or expression microarrays, there has not been an effort to comprehensively sequence these cell lines. Here, we present raw whole transcriptome data generated by RNA sequencing of 39 commonly-used neuroblastoma cell lines. This data can be used to perform differential expression analysis based on a genetic aberration or phenotype in neuroblastoma (eg: MYCN amplification status, ALK mutation status, 11q status, sensitivity to pharmacological pertubation). Additionally, we designed this experiment to enable structural variant and/or long-noncoding RNA analysis across these cell lines. Finally, as more DNase/ATAC and histone/transcription factor ChIP sequencing is performed in these cell lines, our RNA-Seq data will be an important complement to inform transcriptional targets as well as regulatory (enhancer or repressor) elements in neuroblastoma.
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Accession Code
GSE165405
Description
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy. Despite recent advances in treatments with intensified chemotherapy regimens, relapse rates and associated morbidities remain high. In this context, metabolic dependencies have emerged as a druggable opportunity for the treatment of leukemia. Here, we tested the antileukemic effects of MB1-47, a newly developed mitochondrial uncoupling compound. MB1-47 treatment in T-ALL cells robustly inhibited cell proliferation via both cytostatic and cytotoxic effects as a result of compromised mitochondrial energy and macromolecule depletion, which severely impair nucleotide biosynthesis. Mechanistically, acute treatment with MB1-47 in primary leukemias promoted AMPK activation and downregulation of mTOR signaling, stalling anabolic pathways that support leukemic cell survival. Indeed, MB1-47 treatment in mice harboring murine NOTCH1-induced leukemias or human T-ALL PDXs led to a potent antileukemic effect with 2-fold extension in survival without overlapping toxicities. Overall, our findings demonstrate a critical role for mitochondrial oxidative phosphorylation in T-ALL and uncover MB1-47-driven mitochondrial uncoupling as a novel therapeutic strategy for the treatment of this disease.
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A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia
Dataset
Mus Musculus, Homo Sapiens
Accession Code
GSE160427
Description
Long-range oncogenic enhancers play an important role in cancer. Yet, it remains unclear whether similar regulation of tumor suppressor genes is relevant. In this context, loss of expression of the tumor suppressor PTEN is associated with the pathogenesis of various cancers, including T-cell acute lymphoblastic leukemia (T-ALL). Here, we demonstrate that PTEN is regulated in T-cells by a distal enhancer (PE), which is targeted by recurrent focal deletions in T-ALL. This highly conserved regulatory element interacts with and transactivates the PTEN promoter. Consistently, PE deletion in T-ALL cells leads to reduced PTEN levels and proliferative advantage. Moreover, PE-null mice show reduced PTEN levels in the thymus and develop NOTCH1-induced T-ALL with faster kinetics. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by Pten loss. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.
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Accession Code
GSE156070
Description
Single cell suspensions of total thymocytes were obtained from Pten enhancer (PE) wild-type or knockout mice. This single-cell suspension was enriched in CD4-CD3- immature thymocyte progenitor cells. CD4-CD3- enriched thymocytes were then mixed 1:1 with single-cell suspensions from total unenriched thymocytes and subsequntly loaded in a 10x Chromium instrument for single-cell RNAseq analyses. Our results revealed Pten levels are signifcantly decreased in CD4-CD8- double negative (DN) thymocytes, CD8+ intermediate single positive (ISP) thymocytes and CD4+CD8+ double positive (DP) thymocytes in PE knockout mice, compared to PE wild-type mice.
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RNAseq in Pten enhancer wild-type or deleted mouse T-ALLs
Dataset
Mus Musculus
Accession Code
GSE150894
Description
C57BL6 mice harboring Pten enhancer (PE) conditional knockout NOTCH1-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of PE. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice. GSEA analysis show a significant enrichment of Pten signature genes, consistent with a role of PE in regulating Pten expression.
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ATAC-seq in NOTCH1-induced mouse T-ALLs
Dataset
Mus Musculus
Accession Code
GSE160620
Description
Here we report the genome-wide open chormatin profile (ATACseq) of a NOTCH1-induced mouse T-cell Acute Lymphoblastic Leukemia
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