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Tracking transcriptional changes in a species-specific manner during experimental hepatoblastoma progression in vivo

ABSTRACT: Tracking transcriptional changes in a species-specific manner during experimental hepatoblastoma progression in vivo

OTHER RELATED OMICS DATASETS IN: GSE101413

PROVIDER: PRJNA394137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5824320.fastq.gz	Fastqsanger.gz
	SRR5824330.fastq.gz	Fastqsanger.gz
	SRR5824321.fastq.gz	Fastqsanger.gz
	SRR5824331.fastq.gz	Fastqsanger.gz
	SRR5824322.fastq.gz	Fastqsanger.gz

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Tracking transcriptional changes in a species-specific manner during experimental hepatoblastoma progression in vivo

Project description:Hepatoblastoma is a primitive liver cancer occurring mainly in infants with defined molecular alterations driving its progression, which is difficult to model in vivo. Here we present a new animal model for hepatoblastoma on the chick chorioallantoic membrane (CAM), which recapitulates relevant features of hepatoblastoma in patients. Expression of classic tumor-associated proteins such as β-catenin, EpCAM and CK19 was maintained in acini-like organized tumors on CAM, as was synthesis of AFP, a tumor marker used for monitoring patient response. RNA sequencing revealed an unexpected molecular evolution of hepatoblastoma cells on the CAM, with significant deregulation of more than 6000 genes including more than half of all HOX genes. Bioinformatic analysis could clearly distinguish between tumor cell-expressed genes and chick host genes, thereby shedding new light on the complex interactions taking place during experimental hepatoblastoma progression. Importantly, human tumor suppressive ribosomal genes were downregulated after implantation, whereas mitochondrial genes encoding for anti-apoptotic peptides were strongly induced in vivo. Meprin-1α expression was increased during evolution of CAM tumors and confirmed by immunohistochemistry. Cisplatin, a commonly used chemotherapeutic agent for hepatoblastoma, showed significant anti-tumoral effects in this model. Our results broaden the understanding of the molecular adaptation process of human cancer cells to the microenvironment and might help to elaborate novel therapeutic concepts for the treatment of this pediatric liver tumor.

2018-04-17 | GSE101413 | GEO

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Tracking cellular and molecular changes in a species-specific manner during experimental tumor progression in vivo.

Project description:Hepatoblastoma (HBL) is a pediatric liver cancer with defined molecular alterations driving its progression. Here, we describe an animal model for HBL on the chick chorioallantoic membrane (CAM), which recapitulates relevant features of HBL in patients. Expression of classic tumor-associated proteins such as ?-catenin, EpCAM and CK19 was maintained in acini-like organized tumors on CAM, as was synthesis of AFP, a tumor marker used for monitoring patient response. RNA sequencing revealed an unexpected molecular evolution of HBL cells on the CAM, with significant deregulation of more than 6,000 genes including more than half of all HOX genes. Bioinformatic analysis distinguish between tumor cell-expressed genes and chick genes, thereby shedding new light on the complex interactions taking place during HBL progression. Importantly, human tumor suppressive ribosomal genes were downregulated after implantation, whereas mitochondrial genes encoding for anti-apoptotic peptides were strongly induced in vivo. Meprin-1? expression was increased during evolution of CAM tumors and confirmed by immunohistochemistry. Cisplatin, a commonly used chemotherapeutic agent for HBL, showed significant anti-tumoral effects. Our results broaden the understanding of the molecular adaptation process of human cancer cells to the microenvironment and might help to elaborate novel therapeutic concepts for the treatment of this pediatric liver tumor.

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Hepatic transcriptome of pediatric hepatoblastoma.

Project description:The mechanisms underlying hepatoblastoma are not well defined. To address this, we generated transcriptomic profiles of normal, background, and hepatoblastoma liver samples from patients aged 0.01 months to 6 years, using RNA-sequencing. Hepatoblasoma was histologically confirmed. Here we focus on the elevation of stem cell markers and the loss of tumor suppressor proteins leading to the development of hepatoblastoma in very young children.

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Project description:We performed a genome-wide analysis of lncRNA expression in hepatoblastoma tissues to identify novel targets for further study of hepatoblastoma.We found that 2736 lncRNAs were differentially expressed in hepatoblastoma tissues. The genome-wide analysis of lncRNA expression in these tissues was performed using a 4 M-CM-^W 180K lncRNA microarray and Sureprint G3 Human lncRNA Chips.Quantitative RT-PCR (qRT-PCR) was performed to confirm these results.

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