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

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

PROVIDER: PRJNA975461 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24709473_1.fastq.gz	Fastqsanger.gz
	SRR24709473_2.fastq.gz	Fastqsanger.gz
	SRR24709474_1.fastq.gz	Fastqsanger.gz
	SRR24709474_2.fastq.gz	Fastqsanger.gz
	SRR24709475_1.fastq.gz	Fastqsanger.gz

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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

Project description:ACSL4-programmed sphingomyelin metabolism rejuvenates tumor-infiltrating T-cells to enhance efficacy of anti-PD-1 immunotherapy (ATAC-seq)

| PRJNA974502 | ENA

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

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

2012-09-19 | GSE40968 | GEO

Enhancing Acsl4 in absence of mTORC2/Rictor drove β-cell dedifferentiation via inhibiting FoxO1 and promoting ROS production

Project description:We here identified Acsl4, a new target of mTORC2, could rescue the impaired β cell proliferation, but not deficient insulin secretion induced by loss of Rictor.

2022-09-26 | GSE138014 | GEO

Acsl4 Determines Ferroptosis Sensitivity by Shaping Cellular Lipid Composition

Project description:Ferroptosis is a form of regulated necrotic cell death controlled by glutathione peroxidase 4 (GPX4). At present, mechanisms that could predict sensitivity and/or resistance and that may be exploited to modulate this form of cell death are needed. We applied two independent approaches, a genome-wide CRISPR-based genetic screen and microarray analysis of ferroptosis-resistant cell lines to uncover acyl-CoA synthetase long-chain family member 4 (Acsl4) as an essential component for ferroptosis execution.

2017-06-01 | GSE86384 | GEO

Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

Project description:Background: Characterized by high incidence, mutilation, and death rate, acute ischemic stroke (AIS) has threatened people’s health seriously. Therefore, there is an urge need for early diagnosis and effective treatment of AIS. The purpose of this study was to clarify the regulatory role and potential molecular mechanism of miR-342-5p and circRNA_0008146 in AIS. Materials and Methods: Small RNA sequencing analysis was performed to screen differentially expressed miRNAs between the AIS and control group. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. The circRNA_0008146 and miRNA expression levels were detected by quantitative real-time PCR. Assay kits were used to determine Fe2+ levels and assess a battery of oxidative stress indicators, including ROS, MDA, LPO, SOD, and GSH/GSSG. The content of ACSL4 was measured by Western blot. The neurobehavioral manifestation was evaluated using the modified Neurological Severity (mNSS) Score, rotarod test, and corner test. TTC staining was employed to detect cerebral infarction volume. Nissl staining was adapted to detect histological change and neuronal damage. Results: RNA sequencing analysis revealed miR-342-5p was significantly downregulated in the plasma of AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic-reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. CircRNA_0008146 acted as a sponge of miR-342-5p, and overexpression of circRNA_0008146 increased brain damage in stroke mice. CircRNA_0008146 contributed to ferroptosis in cerebral infraction via sponging miR-342-5p to regulate ACSL4. Conclusion: CircRNA_0008146/miR-342-5p/ACSL4 axis regulate ferroptosis after cerebral ischemia-reperfusion, which may be a potential therapeutic target for ischemic stroke.

2024-08-08 | GSE254322 | GEO

Short-term intensive fasting rejuvenates erythropoiesis

Project description:Short-term intensive fasting rejuvenates erythropoiesis

| PRJNA827182 | ENA