Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138633 | ENA |
REPOSITORIES: ENA
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Project description:Over expression of PDGF-C in mouse liver resulted in the progression of hepatic fibrosis, steatosis and the development of HCC; this mouse model closely resembles the human HCC that is frequently associated with hepatic fibrosis. Peretinoin (generic name; code, NIK-333), developed by the Kowa Company, (Tokyo, Japan), is an oral acyclic retinoid (ACR) with a vitamin A-like structure that targets the retinoid nuclear receptor. Peretinoin effectively inhibits the progression of hepatic fibrosis and tumors in Pdgf-c Tg mice. Gene expression profiling was evaluated during the progression of hepatic fibrosis and tumors.
2012-10-03 | GSE31431 | GEO
Project description:Over expression of PDGF-C in mouse liver resulted in the progression of hepatic fibrosis, steatosis and the development of HCC; this mouse model closely resembles the human HCC that is frequently associated with hepatic fibrosis. Peretinoin (generic name; code, NIK-333), developed by the Kowa Company, (Tokyo, Japan), is an oral acyclic retinoid (ACR) with a vitamin A-like structure that targets the retinoid nuclear receptor. Peretinoin effectively inhibits the progression of hepatic fibrosis and tumors in Pdgf-c Tg mice. Gene expression profiling was evaluated during the progression of hepatic fibrosis and tumors. After weaning at week 4, Pdgf-c Tg or non-transgenic WT mice were fed a basal diet or a diet containing+0.06% peretinoin respectively. At week 20, mice were sacrificed for the analysis of progression of hepatic fibrosis. At week 48, mice were sacrificed for the analysis of the development of hepatic tumors.
2012-10-03 | E-GEOD-31431 | biostudies-arrayexpress
Project description:Gene expression of human hepatocellular carcinoma cells in response to acyclic retinoid
| PRJNA292317 | ENA
Project description:Acyclic retinoid induction of HepG2 cells Keywords: other
2004-04-03 | GSE931 | GEO
Project description:Aim: Hepatic fibrosis is a major worldwide medical problem and can develop into liver cirrhosis and hepatocellular carcinoma(HCC). Until now, there are no effective drugs for liver ?brosis because the molecular mechanism of progression of liver fibrosis is not fully understood. MicroRNAs (miRNAs) are an important class of small non-coding functional RNAs that play a key role in many biological processes. The purpose of this study was to clarify how the aberrant expression of miRNAs participates in development of the liver fibrosis in rat liver fibrosis model. Methods: Fibrotic and paired normal liver tissues were collected and assesssed by deep sequencing technology. MiRNA pro?ling results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics was used to predict miRNA targets. Results: Nine deregulated miRNAs were induced in porcine serum (PS)-induced hepatic fibrosis versus normal liver. Further analysis revealed several signaling pathways (e.g., gap junction and neuroactive ligand-receptor interaction) may be associated with hepatic fibrogenesis. Conclusion: Several miRNAs are dysregulated in PS-induced hepatic fibrosis and seem to be closely associated with hepatic fibrogenesis. These results provide an experimental basis for understanding the mechanism of hepatic fibrosis. We sequenced two samples, including case and control. Each sample has two replicates.
2015-06-04 | E-GEOD-54028 | biostudies-arrayexpress
Project description:Acyclic retinoid induction of HepG2 cells
2010-06-09 | E-GEOD-931 | biostudies-arrayexpress
Project description:Aim: Hepatic fibrosis is a major worldwide medical problem and can develop into liver cirrhosis and hepatocellular carcinoma(HCC). Until now, there are no effective drugs for liver fibrosis because the molecular mechanism of progression of liver fibrosis is not fully understood. MicroRNAs (miRNAs) are an important class of small non-coding functional RNAs that play a key role in many biological processes. The purpose of this study was to clarify how the aberrant expression of miRNAs participates in development of the liver fibrosis in rat liver fibrosis model. Methods: Fibrotic and paired normal liver tissues were collected and assesssed by deep sequencing technology. MiRNA profiling results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics was used to predict miRNA targets. Results: Nine deregulated miRNAs were induced in porcine serum (PS)-induced hepatic fibrosis versus normal liver. Further analysis revealed several signaling pathways (e.g., gap junction and neuroactive ligand-receptor interaction) may be associated with hepatic fibrogenesis. Conclusion: Several miRNAs are dysregulated in PS-induced hepatic fibrosis and seem to be closely associated with hepatic fibrogenesis. These results provide an experimental basis for understanding the mechanism of hepatic fibrosis.
2015-06-04 | GSE54028 | GEO
Project description:Prevention and treatment options for hepatocellular carcinoma (HCC) are presently limited, underscoring the necessity for elucidating molecular mechanisms underlying HCC development and identifying new prevention and therapeutic targets. We demonstrate a unique precancerous niche that features enhanced p53 pathway, aberrant cytoplasmic p21WAF1/CIP1-expressing hepatocytes, and increased CD8+ T lymphocyte and macrophage infiltration in the livers of Ncoa5+/- mouse model of HCC. Metformin treatment reverses these precancerous features and profoundly reduces tumor incidence. Our data also reveal that a subset of HCC patients with a similar precancerous niche in the adjacent noncancerous livers had a relatively poor prognosis. Our study suggests a perceptible hepatic niche predisposing to HCC development and uncovers new actions of metformin in the prevention and treatment of HCC.
2020-03-28 | GSE110524 | GEO
Project description:Hepatocellular carcinoma is the third leading cause of cancer death worldwide, and it is necessary to elucidate the mechanism of hepatocarcinogenesis. Hepatocellular carcinoma (HCC) has a high mortality rate and develops based on the chronic inflammatory hepatic disease. Therefore, novel prophylactic or therapeutic strategies are required to improve outcome. In this study, influence of diethylnitrosamine (DEN) and retinoic acid (ATRA) on hepatocarcinogenesis was investigated in mouse. These results suggest that the control of NF-κB signaling during the early stage of HCC development is important for the prevention of malignant transformation in hepatocytes.
2014-06-06 | GSE57798 | GEO