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YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RIP-Seq]

ABSTRACT: YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RIP-Seq]

PROVIDER: PRJNA668007 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12784278_1.fastq.gz	Fastqsanger.gz
	SRR12784278_2.fastq.gz	Fastqsanger.gz
	SRR12784279_1.fastq.gz	Fastqsanger.gz
	SRR12784279_2.fastq.gz	Fastqsanger.gz
	SRR12784280_1.fastq.gz	Fastqsanger.gz

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YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RIP-Seq]

Project description:we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival but is dispensable for normal hematopoiesis. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 significantly induces apoptosis, coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia (AML) cells in vitro and in vivo. Loss of YBX1 does not obviously affect normal hematopoiesis. Mechanistically, YBX1 interacts with IGF2BPs and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency promotes mRNA decay in an m6A-dependent manner, which contributes to the defective survival due to YBX1 deletion. Thus, our findings uncover a selective and critical role of YBX1 in maintaining myeloid leukemia survival that might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.

2021-04-01 | GSE159153 | GEO

YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [SLAM-seq]

2021-04-01 | GSE159152 | GEO

YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RNA-Seq]

Project description:we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival but is dispensable for normal hematopoiesis. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 significantly induces apoptosis, coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia (AML) cells in vitro and in vivo. Loss of YBX1 does not obviously affect normal hematopoiesis. Mechanistically, YBX1 interacts with IGF2BPs and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival due to YBX1 deletion. Thus, our findings uncover a selective and critical role of YBX1 in maintaining myeloid leukemia survival that might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.

2021-04-01 | GSE159178 | GEO

YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner

Project description:YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner

| PRJNA667914 | ENA

Anti-Ybx1 RIP-seq to identify target mRNAs of Ybx1 in E13.5 DRG [RIP-seq]

Project description:In order to identify the target mRNAs of the m5C reader protein Ybx1, we carried out anti-Ybx1 RNA Immunoprecipitation(RIP) followed by RNA-sequencing to find out mRNAs that can directly bind by Ybx1. Using EZ-Magna RIPTM RNA-Binding Protein Immunoprecipitation Kit (Millipore), RNA from E13.5 wildtype mouse DRGs was pulled down by rabbit monoclonal anti-Ybx1 (abcam) and sequenced on IIIumina HiSeq3000 platform. The filtered reads were mapped to the mouse reference genome (GRCm39) using BWA mem (v 0.7.12). After peak calling using MACS2 (version 2.1.0) software, the distribution of chromosome distribution, peak width, fold enrichment, significant level and peak summit number per peak were all displayed. Fold enrichment greater than 2 was considered to be enriched. Finally, 2 biological repilicates of anti-Ybx1 RIP-seq identified 2487 transcripts. This study provides a gene list which shows mRNA binding with Ybx1 in mouse DRGs.

2024-11-15 | GSE254854 | GEO

YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RNA-Seq]

Project description:YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [RNA-Seq]

| PRJNA668008 | ENA

YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [SLAM-seq]

Project description:YBX1 is selectively required for maintaining myeloid leukemia cell survival by regulating mRNA stability in an m6A-dependent manner [SLAM-seq]

| PRJNA667827 | ENA

Anti-Ybx1 RIP-seq to identify target mRNAs of Ybx1 in E13.5 DRG [RIP-seq]

Project description:Anti-Ybx1 RIP-seq to identify target mRNAs of Ybx1 in E13.5 DRG [RIP-seq]

| PRJNA1072092 | ENA

RNA-BisSeq for YBX1 RIP in normal T24 cell

Project description:RNA-BisSeq for YBX1 RIP in normal T24 cell

| PRJNA552057 | ENA

Integrated analysis based on RNA immunoprecipitation sequencing (RIP-seq) and m5C methylated RNA immunoprecipitation and sequencing (MeRIP-seq) assays to identify the target genes of NSUN2/YBX1-m5C axis in ESCC progression

Project description:The modification and recognition of 5-methylcytosine (m5C) are involved in the initiation and progression of various tumor types. However, the precise role and potential mechanism of Y-box-binding protein 1 (YBX1) in esophageal squamous cell carcinoma (ESCC) remains unclear. Here, we found that YBX1 was frequently upregulated in ESCC compared with matched nontumor tissues. Gain- and loss-of-function assays showed that YBX1 promoted the proliferation and metastasis of ESCC cells both in vitro and in vivo. Functional studies revealed that NOP2/Sun RNA methyltransferase family member 2 (NSUN2) is a critical RNA methyltransferase that facilitates YBX1-mediated ESCC progression. Mechanistically, integrated analysis based on RNA immunoprecipitation sequencing (RIP-seq) and m5C methylated RNA immunoprecipitation and sequencing (MeRIP-seq) assays identified spermine oxidase (SMOX) as a target gene containing an m5C site in its coding sequence (CDS) region, which coincided well with the binding site of YBX1. Overexpression of SMOX-WT but not SMOX-Mut partially restored the proliferation and invasion ability of ESCC cells curbed by YBX1 knockdown. Moreover, YBX1 activated the mTORC1 signaling pathway by stabilizing SMOX mRNA. Our study revealed that YBX1 promotes ESCC development by stabilizing SMOX mRNA in an m5C-dependent manner, thus providing a valuable therapeutic target for ESCC.

2024-06-05 | GSE249045 | GEO

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