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Next Generation Sequencing from control and CD97 knockdown of glioblastoma stem cells

ABSTRACT: Next Generation Sequencing from control and CD97 knockdown of glioblastoma stem cells

PROVIDER: PRJNA833863 | ENA |

REPOSITORIES: ENA

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Next Generation Sequencing from control and CD97 knockdown of glioblastoma stem cells

Project description:Glioblastoma (GBM) stem cells (GSCs) are largely associated with a poor prognosis of GBM. Although the importance of identifying and validating molecular markers in GBM has been emphasized, single markers covering all GSCs are lacking. Through in vitro antibody screening, in this study, we demonstrated that CD97 identifies GSCs as a novel surface marker. Compared to conventional well-known GSC markers, such as CD133, CD44 and CD15, only CD97 was notably detected in all tested patient-derived GSCs. GBM patients expressing high levels of CD97 experienced worse clinical outcomes, and were predictive of poor overall survival in the public database. CD97 is required for GSC proliferation and self-renewal and was shown to reduce mouse survival with aggressive tumor progression in an orthotopic xenograft model. A comparative transcriptomic analysis revealed that CD97 triggers mTORC2 signaling through Akt (S473) phosphorylation, enhancing the expression of downstream genes, including ARHGAP1, BZW1, and BZW2. Moreover, inhibition of mTORC2 signaling with the pharmacological inhibitor JR-AP2-011 suppressed GSC proliferation, self-renewal, and downstream gene expression. Furthermore, sorting of CD97-enriched cells from patient-derived GSCs revealed that CD97 promotes GSC self-renewal and tumorigenicity via mTORC2/AKT signaling. Thus, our findings suggest that CD97 may be a general GSC enrichment marker in GBM and that the CD97-related pathway might serve as a therapeutic target for GBM.

2024-12-03 | GSE201960 | GEO

Next generation sequencing following CUX1 knockdown in erythroblasts

Project description:Next generation sequencing following CUX1 knockdown in erythroblasts

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Next Generation RNA Sequencing of Glioblastoma Cancer Associated Fibrobasts

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Effect of CD97 knockdown or overexpression in patient-derived GBM cultures (PDGCs)

Project description:To investigate differentially expressed genes upon CD97 manipulation in GBM

2023-12-01 | GSE230393 | GEO

Next Generation Sequencing of Ctrl and K562 DROSHA knockdown cells

Project description:Next Generation Sequencing of Ctrl and K562 DROSHA knockdown cells

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Next Generation Sequencing Analyzes Transcriptome after TMEM126A overexpression and knockdown

Project description:Next Generation Sequencing Analyzes Transcriptome after TMEM126A overexpression and knockdown

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Next Generation Sequencing Analysis of control and knockdown of hnRNPU in RKO cells

Project description:We knockdown the control and the hnRNPU gene in the RKO cells, then extracted the total RNAs and performed the next generation sequencing. By comparing sequencing data from control and knockdown of hnRNPU cells,we profield the downstream targets of the hnRNPU gene.

2022-12-10 | GSE141771 | GEO

Next Generation Sequencing of Total RNA of Senescent WI38 Human Fibroblast with and without knockdown of G3BP1

Project description:Next Generation Sequencing of Total RNA of Senescent WI38 Human Fibroblast with and without knockdown of G3BP1

2020-06-04 | GSE151745 | GEO

RNA-sequencing of wild-type, CD97- and Gα13-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type, CD97- and Gα13-deficient (Adgre5-/- and CD11c-cre x Gna13fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. Compared to wild-type cDC2s, CD97- and Gα13-deficient cDC2s differentially expressed many genes, but CD97- and Gα13-deficient cDC2s were almost the same. GSEA showed that Mrtf-a dependent genes were upregulated in CD97- and Gα13-deficient cDC2s, which code for cytoskeleton proteins. These data support that CD97-Gα13 signaling regulates splenic cDC2 motility by the actin cytoskeleton.

2022-03-23 | GSE188828 | GEO

CD97 is a Critical Regulator of Acute Myeloid Leukemia Stem Cell Function

Project description:Despite significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor. Understanding the mechanisms that regulate the development and maintenance of leukemic stem cells (LSC) is important to reveal new therapeutic opportunities. We have identified CD97, a member of the adhesion class of G-protein coupled receptors (GPCRs), as a frequently upregulated antigen of AML blasts that is a critical regulator of blast function. High levels of CD97 correlate with poor prognosis, and silencing of CD97 reduces disease aggressiveness in vivo. In order to analyze the functional pathways associated with CD97 expression, we generated RNA-sequence data from scrambled shRNA transfected (s-shRNA) and CD97 KD human AML cell line HL60, as well as from MLL-AF9 (MA9) transduced GMPs isolated from CD97-/- and WT mice. These phenotypes are due to CD97’s function to promote proliferation, survival, and the maintenance of the undifferentiated state in leukemic blasts. Collectively, our data credential CD97 as a promising therapeutic target on LSCs in AML.

2019-07-30 | GSE135028 | GEO

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