Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metformin reverses a precancerous niche featuring cytoplasmic p21WAF1/CIP1-expressing hepatocytes and prevents hepatocellular carcinoma development

ABSTRACT: Metformin reverses a precancerous niche featuring cytoplasmic p21WAF1/CIP1-expressing hepatocytes and prevents hepatocellular carcinoma development

PROVIDER: PRJNA433926 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6714700_1.fastq.gz	Fastqsanger.gz
	SRR6714700_2.fastq.gz	Fastqsanger.gz
	SRR6714710_1.fastq.gz	Fastqsanger.gz
	SRR6714710_2.fastq.gz	Fastqsanger.gz
	SRR6714720_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 50

Similar Datasets

Metformin reverses a precancerous niche featuring cytoplasmic p21WAF1/CIP1-expressing hepatocytes and prevents hepatocellular carcinoma development

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

Metformin reverses gene expression signautres in hyperglycaemics endothelial cells

Project description:Metformin is a well tolerated and often prescribed treatment for type 2 diabetes. However, the effect of metformin on gene expression in endothelial cells remains unknown. We used RNA-seq to profile gene expression in primary human aortic endothelial cells stimulated with metformin in normoglycaemic and hyperglycaemic conditions. We identified novel pathways in hyperglycaemic endothelial cells that may be involved in the development of endothelial dysfunction. Hyperglycaemic endothelial cells expressed interferon-response pathway genes such as MX1 and IFI27. Transcription factor analysis implicates the activation of STAT1 and IRF1. Co-treatment of hyperglycaemic cells with metformin prevented glucose-dependent changes in gene expression, including interferon response genes. Indeed, the effects of metformin in endothelial cells were dependent on glucose levels. In normoglycaemic cells, metformin subtly regulated changes in gene expression. In contrast, metformin was strongly associated with the reversal of gene expression changes induced by hyperglycaemia.

2019-02-01 | GSE77522 | GEO

RNAseq of C. elegans cultured on metformin sensitive and resistant E. coli strains with and without 50mM metformin treatment.

Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.

2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress

Metformin on human macrophages

Project description:Metformin on human macrophages Human blood derived macrophages were treated with 10micromolar Metformin (Sigma-Aldrich) for 4h

2020-06-27 | GSE153318 | GEO

Metformin mice

Project description:Metformin mice Metagenome

| PRJNA1115982 | ENA

Distinct perturbation of the translatome by the anti-diabetic drug metformin

Project description:Reduced cancer incidence has been reported among type II diabetics treated with metformin. Metformin exhibits anti-proliferative and anti-neoplastic effects associated with inhibition of mTORC1, but the mechanisms are poorly understood. We provide the first genome-wide analysis of translational targets of canonical mTOR inhibitors (rapamycin and PP242) and metformin, revealing that metformin controls gene expression at the level of mRNA translation to an extent comparable to that of canonical mTOR inhibitors. Importantly, metformin's anti-proliferative activity can be explained by selective translational suppression of mRNAs encoding cell cycle regulators via the mTORC1/4E-BP pathway. Thus, metformin selectively inhibits mRNA translation of encoded proteins that promote neoplastic proliferation, motivating further studies of this compound and related biguanides in cancer prevention and treatment. MCF7 cells were treated with rapamycin, metformin or PP242 at concentrations that inhibited proliferation to 50% of control. Both cytoplasmic and polysome-associated mRNA was extracted from treatments and a vehicle treated control and probed with microarrays.

2012-05-20 | E-GEOD-36847 | biostudies-arrayexpress

Expression data from mouse liver treated with metformin

Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.

2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress

Metformin regulated genes in human prostate cancer cells

Project description:The biguanide metformin has been shown to not only reduce circulating glucose levels but also suppress in vitro and in vivo growth of prostate cancer. However, the mechanisms underlying the anti-tumor effects of metformin in advanced prostate cancers are not fully understood. The goal of the present study was to define the signaling pathways regulated by metformin in androgen-receptor (AR) positive, castration-resistant prostate cancers. Our group used RNA sequencing (RNA-seq) to examine genes regulated by metformin within the C4-2 human prostate cancer cell line. Western blot analysis and quantitative RT-PCR were used to confirm alterations in gene expression and further explore regulation of protein expression by metformin. Data from the RNA-seq analysis revealed that metformin alters the expression of genes products involved in metabolic pathways, the spliceosome, RNA transport, and protein processing within the endoplasmic reticulum. Gene products involved in ErbB, insulin, mTOR, TGF-, MAPK, and Wnt signaling pathways are also regulated by metformin. A subset of metformin-regulated gene products were genes known to be direct transcriptional targets of p53 or AR. Together, our results suggest metformin regulates multiple pathways linked to tumor growth and progression within advanced prostate cancer cells.

2022-02-10 | GSE196343 | GEO

Metformin Impairs Intestinal Fructose Metabolism

Project description:Objective: To investigate the effects of metformin on intestinal carbohydrate metabolism in vivo. Method: Male mice preconditioned with a high-fat, high-sucrose diet were treated orally with metformin or a control solution for two weeks. Fructose metabolism, glucose production from fructose, and production of other fructose-derived metabolites were assessed using stably labeled fructose as a tracer. Results: Metformin treatment decreased intestinal glucose levels and reduced incorporation of fructose-derived metabolites into glucose. This was associated with decreased intestinal fructose metabolism as indicated by decreased enterocyte F1P levels and diminished labeling of fructose-derived metabolites. Metformin also reduced fructose delivery to the liver. Proteomic analysis revealed that metformin coordinately down-regulated proteins involved carbohydrate metabolism including those involved in fructolysis and glucose production within intestinal tissue. Conclusion: Metformin reduces intestinal fructose metabolism, and this is associated with broad-based changes in intestinal enzyme and protein levels involved in sugar metabolism indicating that metformin's effects on sugar metabolism are pleiotropic.

2024-04-27 | PXD041833 | JPOST Repository

Metformin in fetal hepatocytes

Project description:Fetal sheep hepatocytes were treated for 24h with metformin

2023-02-07 | GSE224387 | GEO