SnRNAseq of bCat-Kras tumors in normal and NASH diet
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1010346 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Current models of hepatocellular tumorigenesis propose that the chronic injury and inflammation in NASH are mutagenic and growth promoting which can eventually lead to HCC. However, contrary to this model, here we show that NASH suppresses the early development of liver cancers in mice. We found that NASH did not hinder the malignant reprogramming of oncogene expressing hepatocytes but suppressed their clonal expansion and led to their elimination. This elimination was not caused by a direct effect of NASH on malignant cells but due to the stimulation of cell competition in tumor-surrounding hepatocytes. Mechanistically, NASH activated the Hippo pathway effectors Yap and Taz in hepatocytes, which elevated their cellular fitness. Thus, deletion of Yap/Taz in tumor-surrounding hepatocytes abolished the elimination of tumor cells by NASH, while experimental hyperactivation of Yap in malignant cells protected them from NASH-induced elimination
2025-09-01 | GSE241856 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays
2011-07-12 | E-MEXP-3291 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.
2022-05-09 | E-MTAB-11688 | biostudies-arrayexpress
Project description:Exosomal microRNA expression profiles of NASH: normal vs. NASH
| PRJNA834825 | ENA
Project description:Transcriptiional profling of 13 normal lung samples, 18 lung KRAS(G12V) tumor samples, and 18 lung HER2(V659E) tumor samples 13 normal lung samples, 18 lung KRAS(G12V) tumor samples, and 18 lung HER2(V659E) tumor samples hybridized against Stratagene universal mouse reference RNA with dye swap
2009-11-30 | E-GEOD-18784 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) is a predominant form of chronic liver disease, affecting nearly 25 % of the global population. The progression from steatosis to nonalcoholic steatohepatitis (NASH) in NAFLD patients is one of the major causes of liver-related death worldwide. We assessed the miRNA expression profiles of the exosomes derived from the peripheral blood of NASH patients or healthy controls.
2022-06-01 | GSE202167 | GEO
Project description:Whole liver from mice with diet-induced nonalcoholic fatty liver disease (NASH) was subjected to bulk RNA-seq. Ingenuity pathway analysis implicated pathways related to the leukocyte adhesion and differentiation in the pathogenesis of NASH. Among the adhesion molecules expressed in endothelial cells, only Icam1 (Log2FC: 1.99; FDR: 1.55E-37) and Vcam1 (Log2FC: 1.93; FDR: 9.32E-35) were differentially upregulated in NASH liver.
2021-02-01 | GSE164084 | GEO
Project description:Human genetic studies have identified several MARC1 variants as protective against non-alcoholic fatty liver diseases (NAFLD). The MARC1 variants are associated with reduced lipid profiles, liver enzymes, and liver-related mortality. However, the role of mitochondrial amidoxime reducing component 1 (mARC1), encoded by MARC1, in NAFLD is still unknown and the therapeutic potential of this target has never been developed. Given that mARC1 is mainly expressed in hepatocytes, we developed an N-acetylgalactosamine conjugated mouse mARC1 siRNA to address this. In ob/ob mice, knockdown of mARC1 in mouse hepatocytes resulted in decreased liver weight, serum lipid enzymes, low-density lipoprotein cholesterol, and liver triglycerides. Loss of mARC1 also improved the lipid profiles and attenuated liver pathological changes in two diet-induced nonalcoholic steatohepatitis (NASH) mouse models. A comprehensive analysis of mARC1-deficient liver in NASH by metabolomics, proteomics, and lipidomics showed that mARC1 knockdown partially restored metabolites and lipids altered by diets. Taken together, loss of mARC1 protects mouse liver from NASH, suggesting a potential therapeutic approach of NASH by downregulation of mARC1 in hepatocytes.
2023-04-28 | MSV000091820 | MassIVE
Project description:Transcriptiional profling of 13 normal lung samples, 18 lung KRAS(G12V) tumor samples, and 18 lung HER2(V659E) tumor samples
2009-12-01 | GSE18784 | GEO
Project description:BACKGROUND & AIMS: Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. METHODS: Microarray was performed to identify differentially expressed genes in NASH. Quantitative real time PCR (qRT-PCR) was used to examine gene expression levels. Western blotting and immunofluorescence staining were employed to examine hemoglobin proteins. Flow cytometry was used to measure intracellular oxidative stress. RESULTS: Analysis of microarray gene expression data has revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopspies from NASH patients. Increased hemoglobin expression in NASH was validated by qRT-PCR. However, the expression of erythrocyte specific marker genes such as SPTA, SPTB, GYPA, GATA1, and ALAS2 did not change, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, induced a dose dependent increase in HBA1 expression in HepG2 cells. Intriguingly, forced hemoglobin expression suppressed oxidative stress. CONCLUSIONS: Oxidative stress upregulates hemoglobin expression in hepatocytes. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage. These findings suggest that hemoglobin is an inducible antioxidant in hepatocytes in response to increased oxidative stress as found in NASH livers. Twelve biopsy diagnosed NASH patients were included in this study. For control groups, total RNA from 5 different subjects were purchased from ADMET. These subjects are free from liver disease.
2010-10-20 | E-GEOD-24807 | biostudies-arrayexpress