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Poly I:C-priming of adipose-derived mesenchymal stromal cells promotes a pro-tumorigenic phenotype in an immunocompetent mouse model of prostate cancer

ABSTRACT: Poly I:C-priming of adipose-derived mesenchymal stromal cells promotes a pro-tumorigenic phenotype in an immunocompetent mouse model of prostate cancer

PROVIDER: PRJNA1028597 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26396932_1.fastq.gz	Fastqsanger.gz
	SRR26396932_2.fastq.gz	Fastqsanger.gz
	SRR26396933_1.fastq.gz	Fastqsanger.gz
	SRR26396933_2.fastq.gz	Fastqsanger.gz
	SRR26396934_1.fastq.gz	Fastqsanger.gz

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Poly I:C-priming of adipose-derived mesenchymal stromal cells promotes a pro-tumorigenic phenotype in an immunocompetent mouse model of prostate cancer

Project description:While BM-MSC remain the most commonly studied MSC subtype and were the focus of original MSC polarization paradigm reports, MSC derived from other tissues may provide advantages for clinical use such as higher relative abundance and differential functional potential. In our previous work, we had identified phenotypical and functional consequences of TLR3 or TLR4 priming on ASC that partially resembled those previously reported for BM-MSC. In our assessment, LPS-priming of ASC rendered them immunostimulatory in immune killing assay coculture assays in the presence of human prostate adenocarcinoma cells and stimulated peripheral blood mononuclear cells. Understanding that tumorigenesis is a complex process involving many other tumor microenvironment components and other supportive tissues, we aimed to evaluate the consequences of TLR-priming in an immunocompetent model of androgen independent prostate cancer by assessing changes in tumor progression, gene expression and immune composition of tumors treated with TLR-primed ASC. The present work expands upon the impact of primed ASC on the prostate tumor microenvironment.

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Poly I:C-priming of adipose-derived mesenchymal stromal cells promotes a pro-tumorigenic phenotype in an immunocompetent mouse model of prostate cancer.

Project description:Introduction: Mesenchymal stromal cells (MSC) are envisioned as a potential cellular vehicle for targeted cancer therapies due to their tumor tropism and immune permissiveness. An obstacle in their use is the duality in their interactions within tumors, rendering them pro-tumorigenic or anti-tumorigenic, in a context dependent manner. MSC preconditioning, or priming, has been proposed as a strategy for directing the effector properties of MSC at tumor sites. Methods: We primed human MSC derived from adipose tissues (ASC), a clinically advantageous MSC source, utilizing toll-like receptor agonists. Subsequently, we explored the consequences in tumor progression and transcriptome upon the interaction of tumor cells with primed or unprimed ASC in an in vivo model of prostate cancer, the second most common cancer and second leading cause of cancer related death in men in the USA. Results and discussion: In the studied model, poly I:C-primed ASC were found to significantly accelerate tumor growth progression. And while unprimed and LPS-primed ASC did not exert a significant effect on tumor growth at the macroscopic level, gene expression analyses suggested that all treatments promoted distinct modulatory effects in the tumor microenvironment, including altered modulation of angiogenesis, and immune response processes. However, the effects resulting from the collective interaction across these processes must be sufficiently skewed in a pro-tumorigenic or anti-tumorigenic direction for evidence of tumor progression modulation to be detectable at the macroscopic level. Our study highlights potential MSC-tumor microenvironment interactions that may be leveraged and should be considered in the development of cancer therapeutics utilizing MSC.

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

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