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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

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

ORGANISM(S): Mus musculus

PROVIDER: GSE283772 | GEO | 2024/12/31

REPOSITORIES: GEO

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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.

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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

Project description:Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

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

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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.

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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).

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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.

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

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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

Nrf1 deficiency promotes tubular ferroptosis by regulating ACSL4 in cisplatin-induced acute kidney injury

Project description:Nrf1 is a transcription factor that is highly conserved and reacts to oxidative, proteotoxic and endoplasmic reticulum stress in cells; nonetheless, its function in the context of acute kidney injury (AKI) remains unclear. Using a model of cisplatin-induced nephrotoxicity in vitro and in vivo, we found that the expression of Nrf1, which is expressed at high levels in renal tubular cells, was significantly downregulated after cisplatin treatment. Proximal tubule-specific Nrf1 knockout worsened and Nrf1 overexpression attenuated cisplatin-induced (CI)-AKI. RNA sequencing analysis revealed that Nrf1 overexpression decreased the number of transcripts involved in cell death, specifically those associated with ferroptosis, after cisplatin treatment. Furthermore, ferroptosis responses, characterized by increased lipid peroxidation and iron content and decreased FPN, XCT and glutathione peroxidase 4 levels, were attenuated in Nrf1-overexpressing HK-2 cells but worsened in Nrf1-knockout mice and Nrf1-knockdown HK-2 cells. Moreover, lipidomic and RNA sequencing results indicated that Nrf1 regulated the levels of polyunsaturated fatty acids (PUFAs) and inhibited the expression of ACSL4. Additionally, ChIP experiments revealed that Nrf1 bound to the promoter region of ACSL4, thereby inhibiting its transcription. Furthermore, inhibitors of ACSL4 significantly reduced the sensitivity of HK-2 cells to ferroptosis induced by Nrf1 knockdown. Collectively, these findings suggest that Nrf1 is a novel target for inhibiting ferroptosis in renal tubule cells by suppressing the transcription and expression of ACSL4, thereby reducing PUFA levels. Consequently, activators developed for Nrf1 may hold therapeutic potential in the treatment of patients with CI-AKI.

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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

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