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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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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

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

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

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

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