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Tumor-derived Lysophosphatidic Acid Blunts Protective Type-I Interferon Responses in Ovarian Cancer

ABSTRACT: Tumor-derived Lysophosphatidic Acid Blunts Protective Type-I Interferon Responses in Ovarian Cancer

PROVIDER: PRJNA754392 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15443822_1.fastq.gz	Fastqsanger.gz
	SRR15443822_2.fastq.gz	Fastqsanger.gz
	SRR15443823_1.fastq.gz	Fastqsanger.gz
	SRR15443823_2.fastq.gz	Fastqsanger.gz
	SRR15443824_1.fastq.gz	Fastqsanger.gz

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Tumor-derived Lysophosphatidic Acid Blunts Protective Type-I Interferon Responses in Ovarian Cancer

Project description:Lysophosphatidic acid (LPA) is a bioactive lipid enriched in highly immunosuppressive neoplasms like ovarian cancer (OvCa). While LPA is known to enhance the tumorigenic capacity of malignant cells, the immunomodulatory role of this phospholipid in cancer remains largely unexplored. Here, we report that LPA operates as a negative regulator of type-I interferon (IFN) responses in OvCa. Ablation of the LPAgenerating enzyme autotaxin in OvCa cells reprogrammed the tumor immune microenvironment, extended host survival, and improved the effects of therapies that elicit protective responses driven by type-I IFN. Mechanistically, LPA sensing by dendritic cells triggered PGE2 synthesis that suppressed type-I IFN signaling via autocrine EP4 engagement. Moreover, we identified an LPA-controlled, immune-derived gene signature associated with weak responses to combined PARP inhibition and PD-1 blockade in OvCa patients. Controlling LPA production or sensing in tumors may therefore be useful to improve cancer immunotherapies that rely on robust induction of type-I IFN.

2022-08-02 | GSE182062 | GEO

Tumor-Derived Lysophosphatidic Acid Blunts Protective Type I Interferon Responses in Ovarian Cancer.

Project description: Not available

| S-EPMC9357054 | biostudies-literature

Investigation of the direct activity of interferon epsilon on ID8 ovarian cancer cells in vitro.

Project description:This experiment is part of a larger study examining the anti-tumour properties of interferon epsilon in ovarian cancer. The objective of this experiment was to examine the direct activity of interferon epsilon on the mouse ovarian cancer cell line, ID8, and compare it to equivalent unit concentrations of interferon beta. The goal was to determine whether interferon epsilon and interferon beta induce different patterns of gene expression in ID8 cells.

2023-03-28 | GSE201345 | GEO

Investigation of the anti-tumour properties of interferon epsilon in high grade serous ovarian cancer in vivo.

Project description:This experiment is part of a larger study examining the anti-tumour properties of interferon epsilon in ovarian cancer. The goal of this experiment was to test the direct effects of interferon epsilon and interferon beta on human ovarian tumours in vivo, using patient derived xenografts (PDX) in immunocompromised (NSG) mice.

2023-03-28 | GSE201337 | GEO

Tumor-intrinsic ST3GAL3 Activity Blunts Anti-tumor Immune and Drives Immunotherapy Resistance in Ovarian Cancer

Project description:Tumor-intrinsic ST3GAL3 Activity Blunts Anti-tumor Immune and Drives Immunotherapy Resistance in Ovarian Cancer

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Spleen vs Lysophosphatidic Acid Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Lysophosphatidic Acid labeled with Cy5- time course with repeats Keywords: ordered

2003-04-14 | GSE388 | GEO

Investigation of the direct activity of type I interferon on Ifnar1 KO ID8 ovarian cancer cells in vitro.

Project description:This experiment is part of a larger study examining the anti-tumour properties of interferon epsilon in ovarian cancer. The goal of this experiment was to assess whether interferon signalling had been ablated in Ifnar1 CRISPR knockout (KO) ID8 cell lines, so that they could be used for in vivo models of ovarian cancer.

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SFRP4 promotes autophagy and blunts FSH responsiveness through inhibition of AKT signaling in ovarian granulosa cells

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Hepatic AKAP1 Deficiency Exacerbates Diet-Induced MASLD by Enhancing GPAT1-mediated Lysophosphatidic Acid Synthesis

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD), closely associated with obesity, can progress to metabolic dysfunction-associated steatohepatitis when the liver undergoes overt inflammatory damage. A-kinase anchoring protein 1 (AKAP1) has been shown to control lipid accumulation in brown adipocytes. However, the role of AKAP1 signaling in hepatic lipid metabolism and MASLD remains poorly understood. Here, we showed that hepatocyte-specific AKAP1 deficiency exacerbated hepatic steatosis and steatohepatitis in male mice subjected to a high-fat diet and fast-food diet, respectively. Mechanistically, AKAP1 directly phosphorylated and inactivated glycerol-3-phosphate acyltransferase 1 (GPAT1) in a PKA-dependent manner, thus suppressing lysophosphatidic acid (LPA) production. Increased endogenous LPA in hepatocytes promoted hepatocellular triglyceride (TG) synthesis and initiated pronounced inflammatory response in Kupffer cells. Restoring hepatic AKAP1 or repressing LPA levels via GPAT1 knockdown alleviated MASLD exacerbation. Overall, AKAP1 plays a protective role against MASLD by inhibiting GPAT1 activity, highlighting the potential of targeting AKAP1/PKA/GPAT1 signalosome for MASLD therapy.

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Boosting NAD+ blunts toll-like receptor-4 induced type I interferon in control and systemic lupus erythematosus monocytes

Project description:Boosting NAD+ blunts toll-like receptor-4 induced type I interferon in control and systemic lupus erythematosus monocytes

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