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

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

PROVIDER: PRJNA667827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12784262_1.fastq.gz	Fastqsanger.gz
	SRR12784262_2.fastq.gz	Fastqsanger.gz
	SRR12784263_1.fastq.gz	Fastqsanger.gz
	SRR12784263_2.fastq.gz	Fastqsanger.gz
	SRR12784264_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 [SLAM-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 | GSE159152 | GEO

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

2021-04-01 | GSE159153 | 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

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 [RIP-Seq]

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

| PRJNA668007 | ENA

YBX1 HITS-CLIP

Project description:In order to identify YBX1 binding sites on endogenous RNA, we performed HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Licatalosi D, et al. 2008, Nature 456:464-U22)

2015-05-08 | E-GEOD-63604 | biostudies-arrayexpress

The MYC-YBX1 Circuit in Maintaining Stem-like Vincristine-Resistant Cells in Rhabdomyosarcoma

Project description:Rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma that causes significant devastation, with no effective therapy for relapsed disease. The mechanisms behind treatment failures are poorly understood. Our study showed that treatment of RMS cells with vincristine led to an increase in CD133-positive stem-like resistant cells. Single cell RNAseq analysis revealed that MYC and YBX1 were among the top-scoring transcription factors in CD133-high expressing cells. Targeting MYC and YBX1 using CRISPR/Cas9 reduced stem-like characteristics and viability of the vincristine-resistant cells. MYC and YBX1 showed mutual regulation, with MYC binding to the YBX1 promoter and YBX1 binding to MYC mRNA. The MYC inhibitor MYC361i synergized with vincristine to reduce tumor growth and stem-like cells in a zebrafish model of RMS. MYC and YBX expression showed a positive correlation in RMS patients, and high MYC expression correlated with poor survival. Targeting the MYC-YBX1 axis holds promise for improving survival in RMS patients.

2023-05-17 | GSE232536 | GEO

YBX1 small-RNA HITS-CLIP

Project description:In order to identify YBX1 binding sites on tRNA fragments, we performed small-RNA HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Chi SW, et al. 2009, Nature 460:479)

2015-05-08 | E-GEOD-63597 | biostudies-arrayexpress

Chip-chip from HCT116 cells with YBX1

Project description:YBX1 is a multifunctional protein involved in the control of transcription and translation. We identified YBX1 as an target of MEK/ERK signaling in colorectal cancer cell lines. We performed a ChIP-chip analysis of HCT116 cells to identify new potential target genes of YBX1. Comparison of input DNA fragments with fragments coprecipitated with YBX1 in HCT116 cells.

2010-10-09 | E-GEOD-18337 | biostudies-arrayexpress

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