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

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

PROVIDER: PRJNA667914 | 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 [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 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

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

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

2021-04-01 | GSE159154 | GEO

YBX1-dependent LNA-tRF-mediated modulation of transcript stability

Project description:In order to identify YBX1-dependent targets that are modulated upon changing the levels of endogenous tRFs, we used transient transfection of antisense locked-nucleic acids (LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr followed by alpha-amanitine treatment, RNA extraction at time points 0 and 8hr post-treatment, and transcriptomic profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected into control and YBX1-knockdown cells to identify YBX1-dependent targets whose stabilities are modulated due to tRF loss-of-function. We used alpha-amanitine mediated inhibition of RNA-polymerase to measure transcript stability across the entire transcriptome.

2015-05-08 | E-GEOD-63565 | biostudies-arrayexpress

YBX1 is required for maintaining myeloid leukemia cell survival by regulating BCL2 stability in an m6A-dependent manner.

Project description:RNA-binding proteins (RBPs) are critical regulators of transcription and translation that are often dysregulated in cancer. Although RBPs are increasingly recognized as being important for normal hematopoiesis and for hematologic malignancies as oncogenes or tumor suppressors, RBPs that are essential for the maintenance and survival of leukemia remain elusive. Here we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival in an N6-methyladenosine (m6A)-dependent manner. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 dramatically induces apoptosis and promotes differentiation coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia cells in vitro and in vivo. Loss of YBX1 has no obvious effect on normal hematopoiesis. Mechanistically, YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1. Thus, our findings have uncovered a selective and critical role of YBX1 in maintaining myeloid leukemia survival, which might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.

| S-EPMC8667054 | biostudies-literature

Ybx1 is required for Survival of Leukemia Stem Cells and the Development of Chronic Myeloid Leukemia

Project description:Chronic myeloid leukemia (CML) is a myeloproliferative disorder derived from hematopoietic stem cells (HSCs) that harbor Philadelphia chromosome (Ph chromosome). Leukemia stem cells (LSCs) in CML are insensitive to TKIs treatment, and are responsible for disease relapse. However, the molecular mechanisms for LSCs survival remains elusive. Here we show that YBX1 plays an important role in regulating survival of CML LSCs. We find that YBX1 expression is significantly increased in CML cells. Using CML patient-derived cell lines and a BCR-ABL-induced CML mouse model, we confirm that YBX1 is required for survival maintenance of LSCs. Deletion of YBX1 impairs the propagation of CML through impairing cell cycle and inducing apoptosis of LSCs. Mechanistically, we find that YBX1 regulates expression of apoptosis-related genes, and YBX1 binds MYC and BCL2 transcripts. YBX1 loss decreases expression of MYC and BCL2 by accelerating their mRNA decay. In addition, restoration of MYC and BCL2 efficiently rescue the defects of YBX1-deficient CML cells. Overall, our findings reveal a critical role of YBX1 in maintaining survival of CML LSCs, which may provide a rationale for targeting YBX1 in CML treatment.

2022-03-27 | GSE199304 | GEO

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