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RNA sequencing of MV4 11 cells harbouring FLT3-ITD mutations

ABSTRACT: RNA sequencing of MV4 11 cells harbouring FLT3-ITD mutations

PROVIDER: PRJNA635291 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11854336_1.fastq.gz	Fastqsanger.gz
	SRR11854336_2.fastq.gz	Fastqsanger.gz
	SRR11854337_1.fastq.gz	Fastqsanger.gz
	SRR11854337_2.fastq.gz	Fastqsanger.gz

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Next generation sequencing identifies small RNA expression in FLT3-ITD+ AML (MV4-11) cell lines

Project description:The expression level of microRNAs in FLT3-ITD+ AML is unknown. Using empty vector (EV) lentiviral CRISPR-Cas9 infected FLT3-ITD+ AML cell lines (MV4-11 cells), we performed next generation RNA sequencing on small RNAs to determine microRNA expression level in these cells. We found a variety of evolutionarily conserved and non-conserved microRNAs expressed in our cells of interest. Small RNAseq on EV lentiviral CRISPR-Cas9 infected MV4-11 cell lines was performed on triplicate cultures.

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Expression profile of wild type (WT) vs miR-155-/- in FLT3-ITD+ AML (MV4-11) cell lines

Project description:The expression profile in miR-155-/- FLT3-ITD+ AML is unknown. Using empty vector (EV) or two distinct miR-155 (S3 or S10) lentiviral CRISPR-Cas9 infected FLT3-ITD+ AML cell lines (MV4-11 cells), we performed next generation RNA sequencing to determine the expression profile in these cells dependent on miR-155. We found a number of pathways dysregulated, including STAT5 activation. RNAseq was performed on EV or miR-155 lentiviral CRISPR-Cas9 infected MV4-11 cell lines in triplicate cultures.

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Next generation sequencing identifies small RNA expression in FLT3-ITD+ AML (MV4-11) cell lines

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Project description:The purpose of the experiment is to investigate whether more co-mutations exists in MV4;11 cells harboring FLT3-ITD/D835 than cells with FLT3-ITD only.

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Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

Project description:This SuperSeries is composed of the SubSeries listed below. The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML cells (primary samples and Ba/F3 cell) and the underlying molecular mechanism of mutation-driven acquired resistance. We identify 310 upregulated and 22 downregulated promoters in FLT3-ITD/D835 mutant AML cells compared to cells with FLT3-ITD (FDR<0.05), and 1945 upregulated and 1470 downregulated promoters in FLT3-ITD/D835 mutant Ba/F3 cells compared to cells with FLT3-ITD.

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Cap analysis gene analysis (CAGE) of Ba/F3 cells harbouring FLT3-ITD mutations (mouse)

Project description:The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML and the underlying molecular mechanism of mutation-driven acquired resistance. We identify 1945 upregulated and 1470 downregulated promoters in FLT3-ITD/D835 mutant Ba/F4 cells compared to cells with FLT3-ITD (FDR<0.05).

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Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

Project description:Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

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Cap analysis gene analysis (CAGE) of primary AML samples harbouring FLT3-ITD mutation (human)

Project description:The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML and the underlying molecular mechanism of mutation-driven acquired resistance. We identify that 310 upregulated and 22 downregulated promoters in FLT3-ITD/D835 mutant AML cells compared to cells with FLT3-ITD (FDR<0.05).

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Genome-wide CRISPR-Cas9 screen identifies protein-coding genes and microRNAs important in FLT3-ITD+ AML (MV4-11) cellular growth

Project description:The functional relevance of many microRNAs in the context of tumor biology remains unclear. Using CRISPR-Cas9 technology, we performed a global loss-of-function screen to test the impact of individual microRNAs on the growth of FLT3-ITD positive leukemia cells. This approach identified both evolutionarily conserved and non-conserved human microRNAs that function to suppress or promote tumor cell growth, revealing that microRNAs are extensively integrated into the molecular networks that control tumor cell physiology. Our study describes a powerful genetic approach by which the function of individual microRNAs can be assessed on a global level, and its use will rapidly advance our understanding of how microRNAs contribute to human disease. Loss-of-function CRISPR-Cas9 screen identifies genes whose loss leads to increased or decreased FLT3-ITD+ cell growth over 23 day time-course

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