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Prom1-deficiency effects on mouse primary hepatocyte transcriptomes in serum-free condition

ABSTRACT: Prom1-deficiency effects on mouse primary hepatocyte transcriptomes in serum-free condition

PROVIDER: PRJNA602515 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919730_1.fastq.gz	Fastqsanger.gz
	SRR10919730_2.fastq.gz	Fastqsanger.gz
	SRR10919731_1.fastq.gz	Fastqsanger.gz
	SRR10919731_2.fastq.gz	Fastqsanger.gz
	SRR10919732_1.fastq.gz	Fastqsanger.gz

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Prom1-deficiency effects on mouse primary hepatocyte transcriptomes in serum-free condition

Project description:Purpose: The function of Prom1, a penta-transmembrane glycoprotein which is a used as cancer stem cell marker, in the liver is unclear. The goal of this study is to examine the effect of Prom1 -/- in mouse primary hepatocyte transcriptomes. Prominin-1 (Prom1) is a major cell surface marker of cancer stem cells, but its physiological functions in the liver have not been elucidated. We analyzed the levels of mRNA transcripts in serum-starved primary Prom1+/+ and Prom1-/- mouse hepatocytes using RNA-sequencing (RNA-seq) data, and found that CREB target genes were down-regulated. This initial observation led us to determine that the Prom1 deficiency inhibited cAMP response element binding protein (CREB) activation and gluconeogenesis, but not cyclic AMP (cAMP) accumulation, in glucagon-, epinephrine-, or forskolin-treated liver tissues and primary hepatocytes, and mitigated glucagon-induced hyperglycemia. Because Prom1 interacted with radixin, the Prom1 deficiency prevented radixin from localizing to the plasma membrane. Moreover, systemic adenoviral knockdown of radixin inhibited CREB activation and gluconeogenesis in glucagon-treated liver tissues and primary hepatocytes, and mitigated glucagon-elicited hyperglycemia. Based on these results, we conclude that Prom1 regulates hepatic PKA signaling via radixin functioning as an A kinase-anchored protein (AKAP).

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Lineage tracing and single-cell analysis reveal proliferative Prom1+ tumor-propagating cells and their dynamic cellular transition during liver cancer progression

Project description:Hepatocellular carcinoma (HCC) is highly heterogeneous, and this heterogeneity contributes to therapeutic resistance and tumor recurrence. The aim of this study was to investigate the role, heterogeneity, and properties of Prom1+ cells in HCC in intact mouse models. We used Prom1C-L/+;Rosa26tdTomato/+ mice to establish two HCC mouse models representing chronic fibrotic HCC and rapid steatosis-related HCC. We performed lineage tracing at different time points post-HCC induction. We ablated the Prom1+ cell population in Prom1C-L/+;Rosa26DTA/+ mice. Single cell RNA-seq (scRNA-seq) was carried out to analyse the lineage properties, heterogeneity, and dynamics of the traced Prom1+ cells in the chronic fibrotic HCC model. Bulk RNAseq was carried out to analyse the change in transcriptome in Prom1 depleted tumor.

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