Homo sapiens strain:HepG2 cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1187001 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31372274_1.fastq.gz | Fastqsanger.gz | |||
| SRR31372274_2.fastq.gz | Fastqsanger.gz | |||
| SRR31372275_1.fastq.gz | Fastqsanger.gz | |||
| SRR31372275_2.fastq.gz | Fastqsanger.gz | |||
| SRR31372276_1.fastq.gz | Fastqsanger.gz |
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Project description:HepG2/C3A cells cultured for 42 h in complete or leucine-devoid medium Experiment Overall Design: Total of 6 Samples (Leu vs noLeu)
2008-11-15 | E-GEOD-13142 | biostudies-arrayexpress
Project description:Transcriptome analysis of LSD2-depleted HepG2 cells revealed that many of the target genes were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. We depleted LSD2 in HepG2 human hepatic cells using three different siRNAs, and then carried out an expression microarray experiment.
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Project description:HepG2/C3A cells cultured for 42 h in complete or leucine-devoid medium
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Project description:Activation of glycolytic genes by HIF-1 is considered critical for metabolic adaptation to hypoxia. We found that HIF-1 also actively suppresses glucose metabolism through the tricarboxylic acid cycle (TCA) by directly trans-activating the gene encoding pyruvate dehydrogenase kinase 1 (PDK1). PDK1 inactivates the TCA cycle enzyme, pyruvate dehydrogenase (PDH), which converts pyruvate to acetyl-CoA. Forced PDK1 expression in hypoxic HIF-1α-null cells increases ATP levels, attenuates hypoxic ROS generation and rescues these cells from hypoxia-induced apoptosis. These studies reveal a novel hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production. Keywords: Hypoxia responsive, case control
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Project description:The mechanistic target of rapamycin complex 1 (mTORC1) is involved in nutrient-induced signaling and is a master regulator of cell growth and metabolism. Amino acid-deficient conditions affect mTORC1 activity; however, its upstream regulators warrant further investigation. MicroRNAs are key regulators of nutrient-related responses; therefore, the present study aimed to assess the leucine starvation-induced microRNA profile and its impact on mTORC1 activity. Transcriptome analysis of human hepatocellular carcinoma cells (HepG2) under leucine deprivation revealed that hsa-miR-663a and hsa-miR-1469 were altered in a transcription factor 4-dependent manner. Overexpression of these microRNAs induced phosphorylation of the ribosomal protein S6 kinase beta-1, a mTORC1 downstream target. Furthermore, hsa-miR-663a downregulated proline-rich Akt1 substrate of 40 kDa (PRAS40), one of the mTORC1 components. In summary, this study provides new insights into the regulatory role of microRNAs in amino acid metabolism and demonstrate alterations in microRNA profile under leucine deprivation in human hepatocytes.
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Project description:Metabolic reprogramming is a hallmark of cancer. Herein we discover that the key glycolytic enzyme pyruvate kinase M2 isoform (PKM2), but not the related isoform PKM1, is methylated by co-activator-associated arginine methyltransferase 1 (CARM1). PKM2 methylation reversibly shifts the balance of metabolism from oxidative phosphorylation to aerobic glycolysis in breast cancer cells. Oxidative phosphorylation depends on mitochondrial calcium concentration, which becomes critical for cancer cell survival when PKM2 methylation is blocked. By interacting with and suppressing the expression of inositol-1,4,5-trisphosphate receptors (InsP3Rs), methylated PKM2 inhibits the influx of calcium from the endoplasmic reticulum to mitochondria. Inhibiting PKM2 methylation with a competitive peptide delivered by nanoparticles perturbs the metabolic energy balance in cancer cells, leading to a decrease in cell proliferation, migration and metastasis. Collectively, the CARM1-PKM2 axis serves as a metabolic reprogramming mechanism in tumorigenesis, and inhibiting PKM2 methylation generates metabolic vulnerability to InsP3R-dependent mitochondrial functions.
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Project description:The proinflammatory cytokine, TNFalpha is critical in maintaining liver homeostasis since it is a major determiner of hepatocyte life and death. Considering this, gene transcription profiling was examined in control and TNFalpha treated HepG2 cells. Results indicated that TNFalpha could significantly alter the expression of a significant number of genes; most of them were functionally distributed among molecular functions like catalytic activity, binding, molecular transducer activity, transporter activity, translation and transcription regulator activities or enzyme regulator activity. Also, within genes up-regulated by TNFalpha, several GO terms related to lipid and fat metabolism were significantly overrepresented indicating global dysregulation of fat metabolism within the hepatocyte and those within the down-regulated dataset included genes involved in immunoglobulin receptor activity and IgE binding thereby indicating a compromise in immune defense mechanism(s) apart from those involved the DNA binding and protein binding categories. The interacting network of “lipid metabolism, small molecule biochemistry” was derived to be significantly affected that correlated well with the top canonical pathway of “biosynthesis of steroids” and molecular and cellular function of “lipid metabolism”. All these indicate TNFalpha to be significantly altering the transcriptome profiling within HepG2 cells with genes involved in lipid and steroid metabolism being the most favoured. This study suitably addresses the genes that determine TNFalpha mediated alterations within the hepatocyte mainly the phenotypes of hepatic steatosis and fatty liver that are associated with several hepatic pathological states. HepG2 cells were maintained in DMEM supplemented with 10% fetal calf serum with 1% antibiotic-antimycotic. On attaining confluency, cells were serum starved overnight and incubated in the absence (control) and presence of TNFalpha (0.5nM, 12h). On termination of incubation, total RNA was isolated, reverse transcribed to cDNA and subjected to in vitro transcription to produce biotinylated cRNA that was hybridized to the human array chip (Human Genome U133 Plus 2.0, Affymetrix) according to the manufacturer's instructions. Images were scanned using the GeneChip 3000 7G scanner (Affymetrix) and analysed. The experiment was performed with triplicates of each set (Control and TNF alpha treated). This experiment was reloaded in November 2010 after additional curation.
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Project description:ChIP-seq analysis of HepG2 cells revealed that many of the target genes of LSD2 were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. Examination of LSD2/DNA interaction in HepG2 cells in normal condition.
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