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RNA-seq of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

ABSTRACT: RNA-seq was performed to assess gene expression alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94853 | GEO | 2017/11/09

SECONDARY ACCESSION(S): PRJNA374790

REPOSITORIES: GEO

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450k methylation array of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

Project description:Methylation profiling was performed to assess methylation alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.

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SOX2 promoter 4C-seq of H9-hESC derived human neural stem cells with mutant IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown

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H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

Project description:H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

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H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-11-09 | GSE94962 | GEO

Detection of ATRX and IDH1-R132H immunohistochemistry in the progression of 211 paired gliomas.

Project description:Recurrence and progression to higher grade lesions are key biological events and characteristic behaviors in the evolution process of glioma. A small residual population of cells always escapes surgery and chemoradiation, resulting in a typically fatal tumor recurrence or progression. IDH mutation (isocitrate dehydrogenase) and ATRX (alpha-thalassemia/mental retardation, X-linked) loss/mutation occur in association and may represent early genetic alterations in the development of gliomas. However, their prognostic value in the evolution of gliomas still needs further investigation.Two hundreds and eleven serial sampling of gliomas were included in our study. We used immunohistochemistry (IHC) to detect IDH1-R132H mutation and ATRX status and showed that the IDH1-R132H and (or) ATRX status could be necessary to provide the basic molecular information for the "integrated diagnosis" of gliomas. We illustrated an evaluation formula for the evolution of gliomas by IDH1-R132H combined with ATRX immunohistochemistry and identified the association of IDH1-R132H/ATRX loss accompanied by longer progression time interval of patients with gliomas. Furthermore, we observed that most recurrences had a consistent IDH1 and ATRX status with their matched primary tumors and demonstrated the progressive pattern of grade II astrocytoma/oligodendroglial tumors and anaplastic oligoastrocytoma with or without IDH1-R132H. Identification of IDH1-R132H and ATRX loss status in the primary-recurrent gliomas may aid in treatment strategy selection, therapeutic trial design, and clinical prognosis evaluation.

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Transcriptional analysis of co-occuring ATRX deficiency and IDH1 mutation in a CT2A glioma model

Project description:Stimulating the innate immune system has been explored as a therapeutic option for the treatment of gliomas. Inactivating mutations in ATRX, a defining molecular alteration in IDH-mutant astrocytomas, have been implicated in dysfunctional immune signaling. However, little is known about the interplay between ATRX loss and IDH mutation on innate immunity. To explore this biology, we generated ATRX knockout glioma models in the presence and absence of the IDH1R132H mutation. ATRX-deficient glioma cells were sensitive to dsRNA-based innate immune agonism and exhibited impaired lethality and increased T-cell infiltration in vivo. However, the presence of IDH1R132H dampened baseline expression of key innate immune genes and cytokines in a manner restored by genetic and pharmacological IDH1R132H inhibition. IDH1R132H co-expression did not interfere with the ATRX KO-mediated sensitivity to dsRNA. Thus, ATRX loss primes cells for recognition of dsRNA, while IDH1R132H reversibly masks this priming. This work reveals innate immunity as a therapeutic vulnerability of astrocytoma.

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Impaired gene expression in ATRX-depleted cells following interferon signaling

Project description:We investigated the role of the chromatin remodeling protein ATRX on ISG expression upon stimulation with IFN-β utilizing doxycycline-inducible ATRX knockdown cells.

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Non-IDH1-R132H IDH1/2 mutations are associated with increased DNA methylation and improved survival in astrocytomas, compared to IDH1-R132H mutations.

Project description:Somatic mutations in the isocitrate dehydrogenase genes IDH1 and IDH2 occur at high frequency in several tumour types. Even though these mutations are confined to distinct hotspots, we show that gliomas are the only tumour type with an exceptionally high percentage of IDH1R132H mutations. Patients harbouring IDH1R132H mutated tumours have lower levels of genome-wide DNA-methylation, and an associated increased gene expression, compared to tumours with other IDH1/2 mutations ("non-R132H IDH1/2 mutations"). This reduced methylation is seen in multiple tumour types and thus appears independent of the site of origin. For 1p/19q non-codeleted glioma (astrocytoma) patients, we show that this difference is clinically relevant: in samples of the randomised phase III CATNON trial, patients harbouring tumours with IDH mutations other than IDH1R132H have a better outcome (hazard ratio 0.41, 95% CI [0.24, 0.71], p = 0.0013). Such non-R132H IDH1/2-mutated tumours also had a significantly lower proportion of tumours assigned to prognostically poor DNA-methylation classes (p < 0.001). IDH mutation-type was independent in a multivariable model containing known clinical and molecular prognostic factors. To confirm these observations, we validated the prognostic effect of IDH mutation type on a large independent dataset. The observation that non-R132H IDH1/2-mutated astrocytomas have a more favourable prognosis than their IDH1R132H mutated counterpart indicates that not all IDH-mutations are identical. This difference is clinically relevant and should be taken into account for patient prognostication.

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Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

Project description:We investigated the role of the chromatin remodeling protein ATRX on chromatin accessibility specifically upon IFN-β stimulation utilizing stable ATRX knockdown cells.

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Stable STIM1 knockdown in human neural precursors derived from hESC line, H9

Project description:Ca2 + signaling plays a significant role in development of the vertebrate nervous system where it regulates neurite growth as well as synapse and neurotransmitter specification (Rosenberg and Spitzer, 2011). Elucidating the role of Ca2 + signaling in neuronal development has been largely restricted to either small animal models or primary cultures. Here we derived human neural precursor cells (NPCs) from human embryonic stem cells to understand the functional significance of a less understood arm of calcium signaling, Store-operated Ca2+ entry or SOCE, in neuronal development. Human NPCs exhibited robust SOCE, which was significantly attenuated by expression of a stable shRNA-miR targeted towards the SOCE molecule STIM1. Along with the plasma membrane channel Orai, STIM is an essential component of SOCE in many cell types where it regulates gene expression. Therefore, we measured global gene expression in human NPCs with and without STIM1 knockdown. Interestingly, pathways down-regulated through STIM1 knockdown were related to cell proliferation and DNA replication processes whereas post-synaptic signaling was identified as an up-regulated process. To understand the functional significance of these gene expression changes we measured the self-renewal capacity of NPCs with STIM1 knockdown. These demonstrated significantly reduced neurosphere size and number as compared to control cells. Moreover, spontaneous differentiation towards the neuronal lineage was enhanced. These findings demonstrate that STIM1 mediated SOCE in human NPCs regulates gene expression changes, that in vivo are likely to physiologically modulate the self-renewal and differentiation of NPCs.

2018-06-27 | GSE109111 | GEO

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