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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

ABSTRACT: Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

PROVIDER: PRJNA831273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18901606_1.fastq.gz	Fastqsanger.gz
	SRR18901606_2.fastq.gz	Fastqsanger.gz
	SRR18901607_1.fastq.gz	Fastqsanger.gz
	SRR18901607_2.fastq.gz	Fastqsanger.gz
	SRR18901608_1.fastq.gz	Fastqsanger.gz

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

Project description:How to identify subgroups of PCa patients for immune checkpoint therapy (ICT) remains not fully understood. Basic helix-loop-helix family member e22 (Bhlhe22) is upregulated in bone metastatic PCa and drives an immunosuppressive bone TME. Tumoral Bhlhe22 mediates the high expression of colony stimulating factor 2 (CSF2), which results in the infiltration of myeloid-derived suppressor cells (MDSCs) and prolonged immunocompromised T cell status. Here, we reveal the immunosuppressive mechanism of tumoral Bhlhe22 and provide a prospective ICT combination therapeutic for Bhlhe22+ PCa patients.

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

Project description:Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

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Project description:In immunosurveillance, bone-derived immune cells infiltrate the tumor and secrete inflammatory cytokines to destroy cancer cells. However, cancer cells have evolved mechanisms to usurp inflammatory cytokines to promote tumor progression. In particular, the inflammatory cytokine, interleukin-1 (IL-1), is elevated in prostate cancer (PCa) patient tissue and serum and promotes PCa bone metastasis. IL-1 also represses androgen receptor (AR) accumulation and activity in PCa cells, yet the cells remain viable; suggesting that IL-1 may also contribute to AR-targeted therapy resistance. Furthermore, IL-1 and AR protein levels negatively correlate in PCa tumor cells. Taken together, we hypothesize that IL-1 reprograms AR positive (AR+) PCa cells into AR negative (AR-) PCa cells that co-opt IL-1 signaling to ensure AR-independent survival in the inflammatory tumor microenvironment. Thus, we employed RNA sequencing to identify pathways that are modulated by IL-1 concomitant with IL-1-induced AR repression in PCa cells. Comparative analysis of sequencing data from the AR+ LNCaP PCa cell line versus the AR- PC3 PCa cell line reveals an IL-1-conferred gene suite in LNCaP cells that is constitutive in PC3 cells, and includes AR and AR target gene repression and the induction of prosurvival, lineage, and cancer stem cell genes. Bioinformatics analysis of the IL-1 regulated gene suite revealed that inflammatory and immune response pathways are primarily elicited; likely facilitating PCa cell survival in an inflammatory tumor microenvironment. Our data supports that IL-1 reprograms AR+ PCa cells to mimic AR- PCa gene expression patterns that favor AR-targeted treatment resistance and cell survival.

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