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A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

ABSTRACT: A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

PROVIDER: PRJNA773415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16522627_1.fastq.gz	Fastqsanger.gz
	SRR16522627_2.fastq.gz	Fastqsanger.gz
	SRR16522628_1.fastq.gz	Fastqsanger.gz
	SRR16522628_2.fastq.gz	Fastqsanger.gz
	SRR16522629_1.fastq.gz	Fastqsanger.gz

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A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

Project description:Hepatoblastoma (HB) is the most common pediatric liver cancer. Its exclusive occurrence in very young children leads us to investigating whether the immature liver provides a protumorigenic niche to HB development. We employed the single-cell RNA-sequencing (sc-RNAseq) to comprehensively profile the HB tumors and their microenvironment in the orthotopic transplantation models established in postnatal day 5 and 60. We demonstrated that the neonatal liver provides a prometastatic niche to HB development via Cxcl1/Cxcr2 axis-mediated HB-aHSC interaction.

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A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

Project description:A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

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A Developmentally Prometastatic Niche in Neonatal Liver to Hepatoblastoma mediated by Cxcl1/Cxcr2 Axis

Project description:We find that various HB cell lines including HepG2 cells are consistently and considerably more tumorigenic and metastatic in the P5Tx model than in the P60Tx models. Sc-RNAseq of the P5Tx and P60Tx HepG2 models reveals that the P5Tx tumor is more hypoxic and has more activated hepatic stellate cells (aHSCs) in the tumor-surrounding liver which express significantly higher levels of Cxcl1 than those from the P60Tx model. We find these differences are developmentally present in the normal P5 and P60 liver. We show that Cxcl1/Cxcr2 axis mediates HB cell migration and is critical to HB cell survival under hypoxia. Treating HepG2 P60Tx model with recombinant CXCL1 protein induces multifocal intrahepatic and pulmonary metastasis and CXCR2 knockout in HepG2 cells abolishes their metastatic potential in the P5Tx model. Lastly, we show that in metastatic HB patient tumors there is a similar larger population of aHSCs in the tumor-surrounding liver than the localized tumors, and tumor hypoxia is significantly associated with HB patient prognosis.

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