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Cancer-associated fibroblasts serve as decoys to suppress NK cell anti-cancer cytotoxicity

ABSTRACT: Cancer-associated fibroblasts serve as decoys to suppress NK cell anti-cancer cytotoxicity

PROVIDER: PRJNA1036644 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26707500_1.fastq.gz	Fastqsanger.gz
	SRR26707500_2.fastq.gz	Fastqsanger.gz
	SRR26707501_1.fastq.gz	Fastqsanger.gz
	SRR26707501_2.fastq.gz	Fastqsanger.gz
	SRR26707502_1.fastq.gz	Fastqsanger.gz

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Cancer-associated fibroblasts serve as decoys to suppress NK cell anti-cancer cytotoxicity

Project description:Cancer associated fibroblasts (CAFs) are one of the most abundant components of the breast tumor microenvironment (TME) and major contributors to immune modulation in the TME. CAFs are well known to regulate the activity of diverse types of immune cells including T cells, macrophages and dendritic cells, however little is known about their interaction with Natural killer (NK) cells. NK cells constitute an important arm of anti-tumor immunity, yet the regulation of NK cell activity by CAFs in solid tumors is poorly understood. Here we find, using mouse models of cancer and ex-vivo cocultures, that immunosuppressive CAF subsets severely inhibit NK cell cytotoxicity towards cancer cells. We unravel the mechanism by which this suppression occurs, through CAF-mediated downregulation of the NK-surface receptors, Natural Killer Group 2D (NKG2D) and DNAX Accessory Molecule-1 (DNAM-1). Ligands for these receptors are known to be expressed by cancer cells and minimally expressed in healthy tissue. Here we find that CAFs also upregulate ligands for NKG2D and DNAM-1. Ligand-receptor engagement between NK cells and CAFs leads to CAF cytolysis, which in turn diminishes the expression of NKG2D and DNAM-1 on NK cells via a negative feedback loop, and promotes cancer escape from NK cell surveillance. These results reveal a CAF-mediated immunosuppressive mechanism with implications for treatment of solid tumors.

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Synthetic circular miR-21 RNA decoys enhance tumor suppressor expression and impair tumor growth in mice (RNA-Seq)

Project description:Natural and synthetic circular RNAs effectively impair miRNA function. MiR-21-5p is a potent oncomiR presenting ~33% of all miRNAs across cancers, ~41% in lung adenocarcinoma (LUAD), and ~68% in LUAD-derived cells. We validate and identify five main tumor suppressors targeted by miR-21-5p by deletion of the MIR21 locus in LUAD cells. Synthetic, liposome-delivered circular miR-21-5p decoys enhance expression of these tumor suppressors and severely impair tumor cell vitality at low doses. Decoy efficacy is not increased by bulging of miR-21-5p targeting sites, but associated with substantial cellular decoy stability, indicated by a half-life of ~20h. The intraperitoneal application of nanoparticle-delivered miR-21-5p decoys significantly impairs tumor growth in mouse LUAD tumor models. Decoys are well tolerated and were enriched in lung tissue. However, despite low decoy abundance, tumor suppressor expression was only increased in subcutaneous tumors. These findings suggest nanoparticle-delivered circular miRNA decoys as potent therapeutics in cancer treatment.

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2-Phenylmaltol treatment induces cytotoxicity in human cancer cell lines.