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RNAseq-based bladder cancer subtyping and IPA analysis with the xenografts from C57 BL/6J

ABSTRACT: RNAseq-based bladder cancer subtyping and IPA analysis with the xenografts from C57 BL/6J

PROVIDER: PRJNA822619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18579118_1.fastq.gz	Fastqsanger.gz
	SRR18579118_2.fastq.gz	Fastqsanger.gz
	SRR18579119_1.fastq.gz	Fastqsanger.gz
	SRR18579119_2.fastq.gz	Fastqsanger.gz
	SRR18579120_1.fastq.gz	Fastqsanger.gz

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RNAseq-based bladder cancer subtyping and IPA analysis with the xenografts from C57 BL/6J

Project description:To subtype the Triple gene knockout tumor we generated and assess the similiarities with widely used MB49 cells, TKO cells were injected into bladder wall orthtopically and bladder lumen by catheter intravesically in C57 BL/6J, while MB49 intravesical injection as a control. TKO intravesical tumors, TKO orthotopic tumors and MB49 intravesical tumors were collected and sent for RNA-seq analysis. In results, both intravesical TKO and orthotopic TKO tumors demonstrates transcriptome profiles that closely resembled human basal like muscle invasive bladder cancer using a luminal/basal/neuronal classifier. Principal Component Analysis (PCA) across samples demonstrated that MB49 cells had transcriptome profiles that differed significantly from TKO tumors. Hence, this study suggest that the TKO tumors closely resemble basal like human bladder cancer and MB49 exhibited no expression of urothelial markers.

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Project description:Expression arrays comparing Campylobacter jejuni 11168 before and after serial passage in C57 BL/6 IL-10 deficient mice. Transcript abundance was compared between C. jejuni variants during growth in the ceca of C57 BL/6 IL-10 deficient germ-free mice. Unpassaged (p0) C. jejuni 11168 was compared to the same strain after three passages (p3) through the mice. Biological replicates: 4; 2 biological replicates were dye swaps.

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Single cell sequencing of anti-PD-1 treated xenograft from mice bladder urothelium with Trp53, Rb1, PTEN mutations on C57 BL/6J

Project description:To determine the immune mechanism of anti-PD1 therapy, we carried out an anti-PD1 treatment on C57 BL/6J mice bearing mouse bladder urothelial carcinoma with three gene knockout. Anti-PD-1 immunotherapy resulted in a mixed pattern of treatment responses in individual tumors. Then, we performed single cell transcriptome profiling for tumor xenografts from Control IgG, anti-PD-1 non-responders and anti-PD-1 responders group. Duplicate tumors in each group were mixed and sequenced together as one representative sample. In results, we captured 4762 cells from Control IgG group, 4459 cells from anti-PD-1 non-responders group and 4861 cells from anti-PD-1 responders group. identified 8 clusters of immune cells in treated samples (basophils, B cells, dendritic cells, macrophages, monocytes, neutrophils, NK cells, and T cells). Responder xenografts displayed significantly increased immune cell infiltration (15.2%, 742 immune cells / 4861 total cells) compared to the non-responder tumors (10.1%, 452 immune cells/ 4459 total cells, Fisher Exact Test p<0.0001). Specifically, there were more T cells (46/4861 vs 18 /4459, p=0.002), and macrophages (420/4861 vs 287/4459, p=0.002) in responder xenografts than in non-responder xenografts. Compared to control IgG tumors, response tumors exhibited an immune-inflamed phenotype with significant infiltration of T cells and NKT cells, whereas non-responder tumors showed no significant change. The higher percentage of T cells and macrophages tumor infiltration in responders suggests a potential role of innate immune microenvironment for the Immune checkpoint inhibitor (ICI) treatment response. This study provides the insights of immune environments in ICI-treated bladder tumor xenograft on C57 mice.

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