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ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

ABSTRACT: ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

PROVIDER: PRJNA1127521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29532824.fastq.gz	Fastqsanger.gz
	SRR29532825.fastq.gz	Fastqsanger.gz
	SRR29532826.fastq.gz	Fastqsanger.gz
	SRR29532827.fastq.gz	Fastqsanger.gz

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ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

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RNAseq in Acly wild-type or conditional KO mouse T-ALLs

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RNAseq in Acly wild-type or conditional KO mouse T-ALLs

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Project description:C57BL6 mice harboring Acly conditional knockout NOTCH1-ΔE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Acly. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice, either in an acute setting or in long-term survival setting

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Expression data by ACLY knockdown

Project description:De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.

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