Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ACSL4 mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis

ABSTRACT: ACSL4 mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis

PROVIDER: PRJNA1193020 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31567681_1.fastq.gz	Fastqsanger.gz
	SRR31567681_2.fastq.gz	Fastqsanger.gz
	SRR31567682_1.fastq.gz	Fastqsanger.gz
	SRR31567682_2.fastq.gz	Fastqsanger.gz
	SRR31567683_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

ACSL4 mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis

Project description:Triple-Negative Breast Cancer (TNBC) has profound unmet medical need globally for its devastating clinical outcome associated with rapid metastasis and lack of targeted therapies. Recently, lipid metabolic reprogramming especially fatty acid oxidation (FAO) has emerged as a major driver of breast cancer metastasis. Analyzing the expression of major FAO regulatory genes in breast cancer, we found selective overexpression of acyl-CoA synthetase 4 (ACSL4) in TNBC, which is primarily attributed by the absence of progesterone receptor (PR). Loss of ACSL4 function, by genetic ablation or pharmacological inhibition significantly reduces metastatic potential of TNBC. Global transcriptome analysis reveals that ACSL4 activity positively influences the gene expression related to TNBC migration and invasion. Mechanistically, ACSL4 modulates FAO and intracellular acetyl-CoA levels, leading to hyper-acetylation of particularly H3K9ac and H3K27ac marks resulting in overexpression of SNAIL during the course of TNBC metastatic spread to lymph node and lung. Further, human TNBC metastasis exhibits positive correlation among ACSL4, H3K9ac, H3K27ac, and SNAIL expression. Altogether, our findings provide new molecular insights regarding the intricate interplay between metabolic alterations and epigenetic modifications, intertwined to orchestrate TNBC metastasis and posit a rational understanding for the development of ACSL4 inhibitors as a targeted therapy against TNBC.

2024-12-20 | GSE283282 | GEO

RNA-seq data in cardiac tissues from cardiomyocyte-specific Acsl4 knockout mice after transverse aortic constriction

Project description:In order to investigate the differentially expressed genes in Acsl4 knockout after TAC (Transverse aortic constriction) or sham surgery. The experiment was divided to four groups including sham-operated Acsl4 flox/flox mice (FS), sham-operated Acsl4 knockout mice (KS), TAC-operated Acsl4 flox/flox mice (FT), TAC-operated Acsl4 knockout mice (KT) n=3 mice/group. The heart tissue was isolated after 21 days after performing TAC or sham surgery.

2024-08-26 | E-MTAB-14383 | biostudies-arrayexpress

The effect of ACSL4 expression on overall gene expression in breast cancer cell lines

Project description:ACSL4 expression appears to be inversely associated with steroid hormone and growth factor receptor expression in breast cancer and positively correlated with an aggressive breast cancer phenotype. Neither MCF-7 nor SKBr3 cells normally express ACSL4, and when manipulated to do so, develop basal-like characteristics, including increased proliferation, migration and anchorage independent growth. We used an Affymetrix array platform to assess changes in individual gene expression as a function of conditional and stable expression of ACSL4 in MCF-7 and SKBr3 cells. In experiment 1, MCF-7 Tet-ON cells were transfected with ACSL4 cDNA and induced to express ACSL4 by addition of 1ug/ml of doxycycline (A) or vehicle (C) for 72 hours. Three controls (C) and three doxycycline-induced (A) samples were evaluated for gene expression. In experiment 2, MCF-7 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A). In experiment 3, SKBr3 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A).

2012-09-19 | E-GEOD-40968 | biostudies-arrayexpress

ACSL4 effect on renal ischemia-reperfusion (I/R) injury

Project description:Analysis of acute kidney injury (AKI) with knockdown of ACSL4. Results provide insight into the role of ACSL4 in the regulation of ferroptosis.

2022-02-23 | GSE181842 | GEO

Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

Project description:Analysis of knockout ACSL4 gene in mouse colorectal cancer cell line. These results are for the role of the ACSL4 gene in colorectal cancer.

2024-12-31 | GSE283772 | GEO

Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer [T84 cells]

Project description:Analysis of ACSL4 gene knockout in human colorectal cancer cell line. These results confirm the role of the ACSL4 gene in colorectal cancer.

2024-12-31 | GSE284613 | GEO

Fatty acid oxidation protects cancer cells from apoptosis through increasing mitochondrial membrane lipids

Project description:<p>Overcoming resistance to chemotherapies remains a major unmet need for cancers such as triple negative breast cancer (TNBC). Therefore, mechanistic studies to provide insight for drug development are urgently needed to overcome TNBC therapy resistance. Recently, an important role of fatty acid β-Oxidation (FAO) in chemoresistance has been shown. But how FAO might mitigate tumor cell apoptosis by chemotherapy is unclear. Here, we show that elevated FAO activates STAT3 by acetylation via elevated acetyl-CoA. Acetylated STAT3 upregulates expression of long-chain acyl-CoA synthetase 4 (ACSL4), resulting in increased phospholipid synthesis. Elevating phospholipids in mitochondrial membranes leads to heightened mitochondrial integrity, which in turn overcomes chemotherapy-induced tumor cell apoptosis. Conversely, in both cultured tumor cells and xenograft tumors, enhanced cancer cell apoptosis by inhibiting ASCL4 or specifically targeting acetylated-STAT3 is associated with a reduction in phospholipids within mitochondrial membranes. This study demonstrates a critical mechanism underlying tumor cell chemoresistance.</p>

2022-05-31 | MTBLS4709 | MetaboLights

ACSL4-programmed sphingomyelin metabolism rejuvenates tumor-infiltrating T-cells to enhance the efficacy of anti-PD-1 immunotherapy

Project description:To investigate whether the expression of ACSL4 may alter the anti-tumor effecet of T-cells, we conditionally knocked out the Acsl4 gene in mouse T-cells (Acsl4-cKO) as descried in Wang et al. Redox Biol 2022. To further demonstrate the importance of SM in ACSL4-mediated T-cell anti-tumor immunity, we conducted a complementary study by intra-tumoral injection of SM in subcutaneous MC38 tumors inoculated in Acsl4-cKO mice.

2024-05-23 | GSE233204 | GEO

The effect of ACSL4 expression on overall gene expression in breast cancer cell lines

2012-09-19 | GSE40968 | GEO

Transcriptomes of triple-negative breast cancer (TNBC) cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared

Project description:The expression levels of JMJD6 and its correlation with H2A.XY39ph differed in TNBC and non-TNBC cells. In addition, we have previously shown that H2A.XY39ph levels are positively correlated with tumor size, histological grade and advanced TNM stage in breast cancer. To analyze the role of JMJD6 in regulating the characteristics of different subtypes of breast cancer, the transcriptomes of TNBC cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared. We speculate that JMJD6 overexpression cause autophagy pathway activation in TNBC via enhancing ATG genes expression.

2023-10-01 | E-MTAB-6517 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data