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ACSL4 and polyunsaturated lipids support metastatic extravasation and colonization

ABSTRACT: ACSL4 and polyunsaturated lipids support metastatic extravasation and colonization

PROVIDER: PRJNA1174147 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31028800_1.fastq.gz	Fastqsanger.gz
	SRR31028800_2.fastq.gz	Fastqsanger.gz
	SRR31028801_1.fastq.gz	Fastqsanger.gz
	SRR31028801_2.fastq.gz	Fastqsanger.gz
	SRR31028802_1.fastq.gz	Fastqsanger.gz

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ACSL4 and polyunsaturated lipids support metastatic extravasation and colonization

Project description:Metastasis is the leading cause of the cancer-related death. To systemically study the dependent factors impacting cancer metastasis, we conducted serial transplantation to obtain ES-2-MC2-Liver cells, a cell line with high metastatic efficiency. We then performed in vivo CRISPR screen using phosphatase and metabolism-focused sgRNA library and ranked differential targeting genes. For further validating the identified gene essentialities in previous results, we generated a mini-library targeting the top-depleted and -enriched genes in metastatic organs and performed in vivo CRISPR screen on ES-2-MC2-Liver cells and SKHEP1 cells. Notably, polyunsaturated lipids synthase, ACSL4, displayed as the top perturbed hits among the lung-specific metastatic mediators. We also evaluated enzymes involved in unsaturated fatty acids degradation were dispensable for metastatic tumor colonization. Taken together, our results systemically study the mediators of cancer metastasis and established the dual functions of PUFA-lipids in tumor progression and metastasis that may be exploitable for therapeutic development.

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

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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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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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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.

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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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Arginine methyltransferase regulates monocyte extravasation and function

Project description:Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process underlying a variety of innate inflammatory responses across multiple organ systems, which requires rapid responses via post translational modifications (PTM) of proteins. Specifically, methylation of protein by arginine methyltransferases (PRMTs) is an epigenetic PTM implicated in inflammatory responses. However, how methyltransferases drive immune regulation particularly in the lung, the resultant tissue injury and whether this might be of therapeutic value has remained unclear. Here, we demonstrate that PRMT7 was increased in the lung of chronic obstructive pulmonary disease (COPD) patients and positively correlated with tissue injury. Accordingly, in clinically relevant models of COPD, lung fibrosis and skin injury, mice with reduced expression of PRMT7 were protected against disease development, due to decreased recruitment of pro-inflammatory monocytes to the site of injury. Mechanistically, we discovered in monocytes activation of NF-κB/RelA induces PRMT7, promoting mono-methylation of histones, which crucially regulates RAP1A and subsequent adhesion and migration ability. Furthermore, in pro-inflammatory monocytes, ALOX5 derived LTB4 induced ACSL4 expression in lung epithelial cells and consequently sensitized towards ferroptosis, thus aggravating tissue injury. Conclusively, specific targeting of arginine mono-methylation offers yet-unappreciated therapeutic potential against monocyte-driven inflammatory conditions.

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