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ScRNA-seq analysis of SHH medulloblastomas in Math1-Cre/SmoM2 mice with homozygous or heterozygous co-deletion of Bcl2l1 (aka Bcl-xL)

ABSTRACT: scRNA-seq analysis of SHH medulloblastomas in Math1-Cre/SmoM2 mice with homozygous or heterozygous co-deletion of Bcl2l1 (aka Bcl-xL)

PROVIDER: PRJNA1061578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27442100_1.fastq.gz	Fastqsanger.gz
	SRR27442100_2.fastq.gz	Fastqsanger.gz
	SRR27442101_1.fastq.gz	Fastqsanger.gz
	SRR27442101_2.fastq.gz	Fastqsanger.gz
	SRR27442082_1.fastq.gz	Fastqsanger.gz

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scRNA-seq analysis of SHH medulloblastomas in Math1-Cre/SmoM2 mice with homozygous or heterozygous co-deletion of Bcl2l1 (aka Bcl-xL)

Project description:We found that medulloblastomas that form in Smo mutant mice grow more slowly when the animals are genetically engineered so that the gene Bcl2l1 is conditionally deleted in the tumor cells. We undertook this study to define changes in cellular heterogeneity and gene expression patterns in the Bcl2l1-deleted medulloblastomas, compared to medulloblastomas with an intact Bcl2l1 allele.

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Project description:Objectives: The aim of the present study was to analyze the differential gene expression of BCL-xL/BCL2L and the associated genetic, molecular, and biologic functions in pancreatic ductal adenocarcinoma (PDAC) by employing advanced bioinformatics to investigate potential candidate genes implicated in the pathogenesis of PDAC. Materials and Methods: Bioinformatic techniques were employed to build the gene network of BCL-xL, to assess the translational profile of BCL-xL in PDAC, assess its role in predicting PDAC, and investigate the associated biologic functions and the regulating miRNA families. Results: Microarray data extracted from one dataset was incorporated, including 130 samples (PDAC: 69; Control: 61). In addition, the expression level of BCL-xL was higher in PDAC compared to control samples (p < 0.001). Furthermore, BCL-xL demonstrated excellent discrimination (AUC: 0.83 [95% Confidence Intervals: 0.76, 0.90]; p < 0.001) and calibration (R squared: 0.31) traits for PDAC. A gene set enrichment analysis (GSEA) demonstrated the molecular functions and miRNA families (hsa-miR-4804-5p, hsa-miR-4776-5p, hsa-miR-6770-3p, hsa-miR-3619-3p, and hsa-miR-7152-3p) related to BCL-xL. Conclusions: The current findings unveil the biological implications of BCL-xL in PDAC and the related molecular functions and miRNA families.

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