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Hepatic p53 protein level governs liver s sensitivity to drug-induced liver injury

ABSTRACT: Hepatic p53 protein level governs liver s sensitivity to drug-induced liver injury

PROVIDER: PRJNA655234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12387749.fastq.gz	Fastqsanger.gz
	SRR12387750.fastq.gz	Fastqsanger.gz
	SRR12387751.fastq.gz	Fastqsanger.gz
	SRR12387752.fastq.gz	Fastqsanger.gz
	SRR12387753.fastq.gz	Fastqsanger.gz

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Hepatic p53 protein level governs liver s sensitivity to drug-induced liver injury

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Project description:Background and Aims: p53 can limit the self-renewal of stem cells from various tissues. Experimental evidence suggests that deletion of p53 can cooperate with other oncogenic events to induce aberrant self-renewal and transformation of progenitor cells. It is not known whether p53 deletion alone can lead to liver tumor formation. Methods: We used AlfpCre mice for liver-specific deletion of Trp53 in a conditional knockout mouse model to analyze liver carcinogenesis. Results: Here, we show that liver-specific deletion of p53 in mice consistently induces formation of liver carcinoma depicting bilineal differentiation. Freshly isolated p53-/- liver progenitor cells and hepatocytes exhibit chromosomal imbalances and an enhanced clonogenic capacity compared to p53-positive cells or p21-deficient cells. Primary cultures of hepatocytes and liver progenitor cells from p53-/- mice formed tumors with bilineal differentiation when transplanted into immuno-compromised mice. Together, these results indicate that loss of p53 alone is sufficient to induce primary liver cancer with bilineal differentiation originating from chromosomal instable cultured liver progenitor cells or hepatocytes. Conclusions: The study shows that p53-dependent checkpoints inhibit transformation of liver progenitor cells and hepatocytes involving p21-independent mechanisms.

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