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Proteomic analysis of Acly knockdown C3H10T1/2 cells

ABSTRACT: This project includes proteomic data of two types of shAcly knockdown C3H10T1/2 cells versus Negative control cells.Control represens the cell with no other treatment.sh2 and sh3 both represen the cell that be knockdown the Acly.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Lingyun Dai

LAB HEAD: Lingyun Dai

PROVIDER: PXD067834 | Pride | 2026-05-22

REPOSITORIES: Pride

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			Action	DRS
	20240602_LX_control_R1.raw	Raw
	20240602_LX_control_R1.raw.quant	Raw
	20240602_LX_control_R2.raw	Raw
	20240602_LX_control_R2.raw.quant	Raw
	20240602_LX_control_R3.raw	Raw

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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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ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via Î±-ketoglutarate

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