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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE163932 | GEO | 2021/01/13

REPOSITORIES: GEO

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

Project description:We performed 3'-RNA-Sequencing on RNA isolated from human MV4-11 and OCI-AML3 cells which had been treated with DMSO or the FLT3 inhibitor Quizartinib (AC220) to perform differential gene expression analysis.

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

Project description:We performed ChIP-seq on MV4-11 or OCI-AML3 cells which had been treated with DMSO or 5 nM of the FLT3 inhibitor Quizartinib (AC220) to determine the location of ATF4 or RNAPII across the genome.

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

Project description:We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 24 or 48 hours compared to non-depleted conditions in vitro to perform differential gene expression analysis.

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

| PRJNA688227 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

| PRJNA688229 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

| PRJNA688222 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

| PRJNA688230 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

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Oncogenic roles of PRL-3 in FLT3-ITD induced acute myeloid leukaemia.

Project description:FLT3-ITD mutations are prevalent mutations in acute myeloid leukaemia (AML). PRL-3, a metastasis-associated phosphatase, is a downstream target of FLT3-ITD. This study investigates the regulation and function of PRL-3 in leukaemia cell lines and AML patients associated with FLT3-ITD mutations. PRL-3 expression is upregulated by the FLT3-STAT5 signalling pathway in leukaemia cells, leading an activation of AP-1 transcription factors via ERK and JNK pathways. PRL-3-depleted AML cells showed a significant decrease in cell growth. Clinically, high PRL-3 mRNA expression was associated with FLT3-ITD mutations in four independent AML datasets with 1158 patients. Multivariable Cox-regression analysis on our Cohort 1 with 221 patients identified PRL-3 as a novel prognostic marker independent of other clinical parameters. Kaplan-Meier analysis showed high PRL-3 mRNA expression was significantly associated with poorer survival among 491 patients with normal karyotype. Targeting PRL-3 reversed the oncogenic effects in FLT3-ITD AML models in vitro and in vivo. Herein, we suggest that PRL-3 could serve as a prognostic marker to predict poorer survival and as a promising novel therapeutic target for AML patients.

| S-EPMC3799491 | biostudies-literature

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