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Effect of RBM5 knockout or overexpression on transcription in MOLM13 AML cells

ABSTRACT: Effect of RBM5 knockout or overexpression on transcription in MOLM13 AML cells

PROVIDER: PRJNA936855 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23557763_1.fastq.gz	Fastqsanger.gz
	SRR23557763_2.fastq.gz	Fastqsanger.gz
	SRR23557764_1.fastq.gz	Fastqsanger.gz
	SRR23557764_2.fastq.gz	Fastqsanger.gz
	SRR23557765_1.fastq.gz	Fastqsanger.gz

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Effect of RBM5 knockout or overexpression on transcription in MOLM13 AML cells

Project description:Background: The oncogenic protein HOXA9 plays a critical role in leukemia transformation and maintenance, and its aberrant expression is a hallmark of most aggressive acute leukemia. Although inhibiting the upstream regulators of HOXA9 has been proven as a significant therapeutic intervention, the comprehensive regulation network controlling HOXA9 expression in leukemia has not been systematically investigated. Results: Here, we perform genome-wide CRISPR/Cas9 screening in the HOXA9-driven reporter acute leukemia cells. We identify a poorly characterized RNA-binding protein, RBM5, as the top candidate gene required to maintain leukemia cell fitness. RBM5 is highly overexpressed in acute myeloid leukemia (AML) patients compared to healthy individuals. RBM5 loss triggered by CRISPR knockout and shRNA knockdown significantly impairs leukemia maintenance in vitro and in vivo. Through domain CRISPR screening, we reveal that RBM5 functions through a noncanonical transcriptional regulation circuitry rather than RNA splicing, such an effect depending on DNA-binding domains. By integrative analysis and functional assays, we identify HOXA9 as the downstream target of RBM5. Ectopic expression of HOXA9 rescues impaired leukemia cell proliferation upon RBM5 loss. Importantly, acute protein degradation of RBM5 through auxin-inducible degron system immediately reduces HOXA9 transcription. Conclusions: We identify RBM5 as a new upstream regulator of HOXA9 and reveal its essential role in controlling the survival of AML. These functional and molecular mechanisms further support RBM5 as a promising therapeutic target for myeloid leukemia treatment. Keywords: Acute myeloid leukemia; CRISPR screen; Genome editing; HOXA9; RBM5.

2023-11-16 | GSE225633 | GEO

The Effect of RBM5 Gene Manipulation on Expression Data from Day In Vitro 6 Primary Rat Cortical Neurons

Project description:RNA Binding Motif 5 (RBM5) is a nuclear splicing factor. Prior studies show that RBM5 overexpression in cancer cells alters gene splicing, gene expression, and induces cell death and/or growth arrest. The role of RBM5 in primary neurons is unknown, and its potential mRNA targets have not been identified. Using lentivirus based approaches we tested if RBM5 knockdown (i.e. by shRNA) or RBM5 overexpression (DDK-tagged rat open reading frame) alters whole genome expression in primary rat cortical neurons. We used microarrays to examine genes that are up-regulated vs. down-regulation in cortical neurons after RBM5 knockdown vs. overexpression.

2018-02-16 | GSE98858 | GEO

miCLIP, RNA-Seq, and Ribo-Seq in MOLM13 cells

Project description:We studied the following conditions: m6A RNA methylation in MOLM13 AML cells; METTL3 deficiency on gene expression and translational efficiency

2017-09-18 | GSE98623 | GEO

RBM5 and RBM10

Project description:RBM5 and RBM10

| PRJNA1004300 | ENA

RNA-seq identifies differential expressed genes upon YTHDC1 knockdown in MOLM13 human acute myeloid leukemia cells

Project description:The goal of this study is to identify differential expressed genes upon YTHDC1 depletion in MOLM13 cells(AML).

2021-05-24 | GSE168565 | GEO

Effect of Gilteritinib, Metformin and Combination treatments on gene expression in MOLM13-RES cells

Project description:Here, we report that Metformin shows a striking synergistic effect with Gilteritinib in suppressing cell proliferation and promoting apoptosis and cell cycle arrest in multiple FLT3-ITD AML cell lines, including FLT3 TKI-resistant MOLM13 cells. Mechanistically, the combinational treatment synergistically suppresses Polo-like kinase 1 (PLK1) expression and phosphorylation of FLT3/STAT5/ERK/mTOR in MOLM13-RES cells. Intriguingly, our retrospective clinical analysis has unveiled a significant correlation between Metformin intake and improved survival rates among FLT3-ITD AML patients. Collectively, the cotreatment of Metformin and Gilteritinib shows robustly enhanced therapeutic efficacy in treating FLT3-mutated AML by synergistically suppressing PLK1 expression and phosphorylation of FLT3/STAT5/ERK/mTOR.

2024-06-14 | GSE244855 | GEO

Genome-wide maps of AF10( MLLT10) PZP binding in MOLM13 human AML cells

Project description:We report genomic occupancy of the AF10 PZP domain in MOLM13 cells

2020-12-15 | GSE163170 | GEO

Identification of RBM5 and RBM10-dependent splicing events in 293Flp-In cells.

Project description:RBM5 and RBM10 are RNA-binding proteins and splicing regulators. These two proteins are putative paralogs in mammalian cells, sharing common domain organization and extensive protein sequence similarity, but their RNA-binding preferences differ. We developed a sensitive system to identify splicing events regulated by RBM5 and/or RBM10, deleting all RBM5 alleles in 293Flp-In cells, and reducing the expression of RBM10, which is partially rescued by activation of a cryptic exon (CE) in one of the RBM10 alleles. RBM5 or RBM10 transgenes were then introduced in these RBM5-null, RBM10 mutant cells (RBM5-/-;RBM10-/CE), allowing controlled protein expression, induced with Doxycycline. Using this system we identify thousands of RBM5 and RBM10-regulated cassette exons, and note a substantial overlap between the two sets.

2024-03-08 | GSE240259 | GEO

Effect of Ro 08-2750 treatment on gene expression of human leukemia cell lines MOLM13 and K562

Project description:RNA-sequencing on human leukemia cell lines MOLM13 (AML, MLL-AF9+) and K562 (CML-BC, BCR-ABL+) after Ro 08-2750 treatment (20 uM, 4hours)

2019-05-09 | GSE114320 | GEO

Gene expression changes after chemical knockout of ENL in Molm13 cells

Project description:Gene expression changes after chemical knockout of ENL in Molm13 cells

| PRJNA789315 | ENA