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RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RIP-seq]

ABSTRACT: We demonstrated that CELF2 regulates FAT10, and promotes mTORC1 signaling pathway activation in MLL-AF9-AML mice.

ORGANISM(S): Homo sapiens

PROVIDER: GSE217987 | GEO | 2022/11/17

REPOSITORIES: GEO

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RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RNA-seq]

Project description:We demonstrated that CELF2 regulates FAT10, and promotes mTORC1 signaling pathway activation in MLL-AF9-AML mice.

2022-11-17 | GSE217988 | GEO

RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RIP-seq]

Project description:RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RIP-seq]

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RBP CELF2 regulates acute leukemia development via FAT10-mTORC1.

Project description:RBP CELF2 regulates acute leukemia development via FAT10-mTORC1.

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RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RNA-seq]

Project description:RBP CELF2 regulates acute leukemia development via FAT10-mTORC1 [RNA-seq]

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RBP CELF2 regulates acute leukemia development via FAT10-mTORC1.

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

2022-11-17 | GSE217989 | GEO

Expression profiling with RNA-seq between mTORC1 high and low AML cells

Project description:We reported the expression profiling between mTORC1 high and low mouse AML cells with MLL-AF9 utilizing a novel fluorescent probe named mVenus-TOSI (TOr-Signal-Indicator). For this purpose, 3 mTOR high (mVenus low) and 4 mTOR low (mVenus high) Mouse AML cells were harvested from 4 mice. The transcriptomic profiles were distinctive and gene ontology analysis revealed that mTORC1 activity was associated with differentially expressed immune response and metabolism related genes. Further, gene signature enrichment analysis (GSEA) validated that the mTORC1 signal signature correlated with mTORC1 activity and that leukemia stem cell (LSC), Myc, and cell cycle related signatures were enriched in mTORC1 high cells.

2020-11-29 | GSE161362 | GEO

POLR2M-mediated paused transcription silences tumor suppressor MIR139 in MLL-AF9 AML

Project description:MIR139 is a critical tumor suppressor and commonly silenced in human cancer, including acute myeloid leukemia (AML). Here, we found that depletion of identified MIR139 targets affects AML outgrowth. We unraveled the mechanism of MIR139 gene inactivation in AML expressing the Mixed-Lineage Leukemia (MLL)-AF9 oncogene. Epigenetic analyses revealed two well-conserved putative enhancer regions in close proximity of transcriptional start sites (TSS) of MIR139. These regions were silenced by the Polycomb-Repressive Complex-2 (PRC2) downstream of MLL-AF9. Genomic deletion of these regions abolished MIR139 transcriptional regulation in normal and oncogenic conditions. Genome-wide knockout screens revealed the transcriptional pausing factor of RNA Polymerase-II, POLR2M, as a critical MIR139-silencing factor. Furthermore, direct POLR2M binding to the MIR139 TSS induced paused transcription, which was abrogated upon PRC2 inhibition. We present evidence for an oncogenic POLR2M-mediated MIR139 silencing mechanism, downstream of MLL-AF9 and PRC2. Together, our findings highlight the importance of POLR2M-mediated paused transcription in AML.

2021-11-11 | PXD022488 | Pride

RNA-seq profiling of murine Tet-off MLL-AF9; NRAS acute myeloid leukemia at different timepoints upon doxycycline-induced MLL-AF9 down-regulation.

Project description:Using an acute myeloid leukemia (AML) mouse model driven by tet-regulated MLL-AF9 (fusion between the gene MLL1 (KMT2A/MLL) and MLLT3 (AF9)) co-expressed with oncogenic NRASG12D (Tet-off MLL-AF9), we investigated the effect of modulating the expression of the MLL-AF9 fusion oncogene on the transcriptome and proteome of established murine AML. Treatment in vitro or in vivo of these Tet-off MLL-AF9 AMLs with doxycycline (DOX) results in the efficient down-regulation of the expression of the driver oncogene MLL-AF9. RNA sequencing analysis was performed on primary Tet-Off MLL-AF9 AML cells obtained from the spleen of leukemic animals and cultured in vitro for either 2 or 4 days in the presence of doxycycline (1μg/ml) (DOX= down-regulation of MLL-AF9) or left untreated (UT).

2021-12-31 | GSE108326 | GEO

RNA sequencing expression analysis of murine Tet-off MLL-AF9;NRAS acute myeloid leukemia cells over-expressing Id2 and upon MLL-AF9 withdrawal

Project description:We investigated the role of the transcriptional regulator Id2 in the context of MLL-rearranged acute myeloid leukemia (AML). Using an AML mouse model driven by tet-regulated MLL-AF9 co-expressed with oncogenic NRASG12D (Tet-off MLL-AF9), we demonstrated that MLL-AF9 regulates the E protein pathway by suppressing Id2, while activating the expression of its target E2-2. Moreover, we found that Id2 over-expression in Tet-Off MLL-AF9 AML cells in vitro partially phenocopies MLL-AF9 depletion and results inhibition of leukemia growth, loss of leukemia stem cell-associated gene expression pattern and induction of differentiation. To compare gene expression changes associated with enforced Id2 expression and MLL-AF9 withdrawal, RNA sequencing analysis was performed on Tet-off MLL-AF9 cells transduced with an Id2 over-expressing or a control vector, or upon MLL-AF9 dox-inducible knock-down. Primary AMLs driven by Tet-off inducible MLL/AF9 expression linked to dsRED reporter, in association with oncogenic NRASG12D (Tet-off MLL-AF9) were generated by reconstituting lethally irradiated congenic mice with foetal liver cells co-transduced with a Tet-Off-MLL-AF9-dRED retroviral vector and a second vector co-expressing NRASG12D together with the Tet-Off responsive transcriptional activator. RNA sequencing analysis sequencing analysis was performed on Tet-Off MLL-AF9/dsRED+ AML cells treated in vitro with doxycycline (DOX) for 4 days to inactivate MLL-AF9 expression or left untreated (UT). For the Id2 over-expression experiment, Tet-Off MLL-AF9/dsRED+ AML cells were transduced in vitro with an Id2-GFP or a control-GFP retroviral vector. Viable GFP-positive cells were FACS-sorted 2 days after transduction and used for RNA sequencing analysis.

2016-06-29 | E-GEOD-68462 | biostudies-arrayexpress

Tumor suppressive role of CELF2 in skin tumorignesis

Project description:To investigate the function of CELF2 in non-melanoma skin cancer, we performed immunofluorescence staining studies and found lower CELF2 expression in human squamous cell carcinoma (SCC) tumors than in adjacent normal skin. CELF2 expression was also downregulated during both ultraviolet light- and chemical-induced skin tumorigenesis in mice, suggesting that CELF2 loss might promote skin cancer development. By using shRNA-mediated knockdown (KD) of CELF2 expression, we showed that CELF2 deficiency significantly increased SCC cell proliferation and colony growth in vitro and increased SCC tumor growth in a xenograft mouse model. Although control SCC cells were sensitive to anticancer drugs such as doxorubicin, CELF2-KD SCC cells were resistant to drug-induced tumor growth retardation. Through RNA-seq analysis, we identified that CELF2 loss led to activation of KRT80 and GDF15, which could confer growth and survival advantages to CELF2-deficient SCC cells.

2024-12-26 | GSE244862 | GEO

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