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Deep sequencing reveals abundant non-canonical onco-retroviral microRNAs in B-cell leukemia/lymphoma

ABSTRACT: Viral tumor models have significantly contributed to our understanding of oncogenic mechanisms. How transforming delta-retroviruses induce malignancy however remains poorly understood, especially as viral mRNA/protein are tightly silenced in tumors. Here, using deep sequencing of broad windows of small RNA sizes in the Bovine Leukemia Virus ovine model of leukemia/lymphoma, we provide evidence of the production of non-canonical Pol III-transcribed viral microRNAs in leukemic B-cells in the complete absence of Pol II 5' LTR-driven transcriptional activity. Processed from a cluster of five independent self-sufficient transcriptional units located in a proviral region dispensable for in vivo infectivity, BLV microRNAs represent ~ 40 % of all microRNAs in both experimental and natural malignancy. They are conserved across tumors and associate with Argonautes, consistent with a critical function in silencing of important cellular and/or viral targets. BLV microRNAs are strongly expressed at pre-leukemic stages and remain at high levels in malignant cells despite the absence of structural and regulatory gene expression, suggesting a key role in tumor onset and progression.

ORGANISM(S): Ovis aries

PROVIDER: GSE42316 | GEO | 2013/01/24

SECONDARY ACCESSION(S): PRJNA181011

REPOSITORIES: GEO

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Deep sequencing reveals abundant non-canonical onco-retroviral microRNAs in B-cell leukemia/lymphoma

Project description:Viral tumor models have significantly contributed to our understanding of oncogenic mechanisms. How transforming delta-retroviruses induce malignancy however remains poorly understood, especially as viral mRNA/protein are tightly silenced in tumors. Here, using deep sequencing of broad windows of small RNA sizes in the Bovine Leukemia Virus ovine model of leukemia/lymphoma, we provide evidence of the production of non-canonical Pol III-transcribed viral microRNAs in leukemic B-cells in the complete absence of Pol II 5' LTR-driven transcriptional activity. Processed from a cluster of five independent self-sufficient transcriptional units located in a proviral region dispensable for in vivo infectivity, BLV microRNAs represent ~ 40 % of all microRNAs in both experimental and natural malignancy. They are conserved across tumors and associate with Argonautes, consistent with a critical function in silencing of important cellular and/or viral targets. BLV microRNAs are strongly expressed at pre-leukemic stages and remain at high levels in malignant cells despite the absence of structural and regulatory gene expression, suggesting a key role in tumor onset and progression. Identification of small RNA populations in BLV-induced leukemia

2013-01-24 | E-GEOD-42316 | biostudies-arrayexpress

Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization [4C-seq]

Project description:Bovine Leukemia Virus (BLV)-induced tumoral development is a multifactorial phenomenon which remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the BLV provirus. Next, we showed the localization of CTCF to transitions in the histone modifications profile along BLV genome as well as its implication in the repression the 5’Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3’LTR promoter activity. Finally, we demonstrated that BLV integration deregulated host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.

2022-02-18 | GSE178483 | GEO

Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization [ChIP-seq]

2022-02-18 | GSE178482 | GEO

Expression data from Bovine leukemia virus (BLV) Tax-transfected HeLa cells

2013-01-03 | GSE35823 | GEO

Expression data from Bovine leukemia virus (BLV) Tax-transfected HeLa cells

Project description:Bovine leukemia virus (BLV) Tax is a transcriptional activator of viral replication and a key contributor to oncogenic potential. We previously identified interesting mutant forms of Tax with elevated (TaxD247G) or reduced (TaxS240P) transactivation effects on BLV replication and propagation. In this study, to identify genes that play a role in the cascade of signal events regulated by wild-type and mutant Tax proteins, we used a large-scale host cell gene-profiling approach. HeLa cells transiently transfected with the pCAGGS vector for the control sample was compared with HeLa cells transiently transfected with the pCAGGS-Tax-FLAG vector. These cells were incubated for 30h after transfection and total RNA was isolated.

2013-01-03 | E-GEOD-35823 | biostudies-arrayexpress

The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples.

Project description:Acute myeloid leukemia (AML) is a clonal hematopoietic malignancy, characterized by expansion of immature leukemic blasts in the bone marrow. In AML, specific tyrosine kinases have been implicated in leukemogenesis, and are associated with poor treatment outcome. However, targeted therapy using kinase inhibitors (KIs) has had limited success, and may be improved by proper patient selection. We performed phosphotyrosine (pY) based, label-free phosphoproteomics to identify hyperphosphorylated, active kinases in two FLT3+ AML Pt samples.

2020-03-02 | PXD015639 | Pride

Expression data from T-cell Acute Lymphoblastic Leukemia (T-ALL) patient-derived xenograft treated with anti-CD3 mAb

Project description:T-cell acute lymphoblastic leukemia is a hematological malignancy treated by chemotherapy, with a poor prognosis. We have demonstrated that activation of the T cell receptor (TCR) by anti-CD3 antibodies has a potent anti-leukemic effect in patient-derived xenograft models (PDX) of T-ALL. Therefore, with this experiment, we aim to identify the molecular mechanisms underlying the anti-leukemic properties of the OKT3 anti-CD3 mAb in T-ALL PDX.

2024-03-19 | GSE240296 | GEO

The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples-LYSATES.

2020-03-02 | PXD015662 | Pride

Bovine Leukemia Virus (BLV) antisense transcripts

Project description:Characterization of novel Bovine Leukemia Virus (BLV) antisense transcripts by deep sequencing reveals constitutive expression in tumors and transcriptional interaction with viral microRNAs

| PRJEB13872 | ENA

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.

2018-07-11 | GSE116776 | GEO

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