Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NCBP2 promotes colorectal cancer growth and metastasis by driving lipid droplet accumulation by stabilizing LIPG mRNA

ABSTRACT: NCBP2 promotes colorectal cancer growth and metastasis by driving lipid droplet accumulation by stabilizing LIPG mRNA

PROVIDER: PRJNA1126308 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

NCBP2 promotes colorectal cancer growth and metastasis by driving lipid droplet accumulation by stabilizing LIPG mRNA

Project description:RNA-binding proteins are critical for RNA processing and aberrantly expressed in colorectal cancer (CRC). In this study, by screening and bioinformatic analyses of the TCGA database and GSE20916 and GSE18105 datasets, NCBP2 was ultimately identified as a potential oncogene in CRC. We observed that NCBP2 was overexpressed in tumour tissues; its overexpression was correlated with CRC invasion and distant metastasis and indicated poorer survival in CRC patients. NCBP2 overexpression promoted the proliferation, migration and invasion of CRC cells in vitro and in vivo. Mechanistically, the NCBP2 protein stabilizes LIPG mRNA and increases LIPG expression via direct binding to m7G in the 5’-cap structure of LIPG mRNA. NCBP2 also facilitates lipid droplet accumulation in CRC cells in a LIPG-dependent manner. This study demonstrated that the NCBP2–LIPG–lipid droplet axis represents a new mechanism for CRC growth and distant metastasis and is a promising target for CRC treatment.

2024-08-30 | GSE270402 | GEO

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age

| PRJNA1100203 | ENA

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082_28_MASTER]

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082_28_MASTER]

| PRJNA1100202 | ENA

Microglial REV-ERBα regulates inflammation and lipid droplet formation to drive tauopathy

Project description:Alzheimer’s disease is associated with disrupted circadian rhythms and clock gene expression. REV-ERBα (Nr1d1) is a circadian transcriptional repressor involved in the regulation of lipid metabolism and macrophage function. While global REV-ERBα deletion increases microglial activation and mitigates amyloid plaque formation, the cell-autonomous effects of microglial REV-ERBα on tau pathology are unexplored. Here, we show that microglial REV-ERBα deletion enhances inflammatory signaling, disrupts lipid metabolic processes, and causes lipid droplet (LD) accumulation specifically in male microglia. Inflammation and LD accumulation combine to inhibit microglial tau phagocytosis, which can be partially rescued by blockage of lipid droplet formation. Microglial REV-ERBα deletion exacerbates tau aggregation and neuroinflammation in P301S and AAV-P301L tauopathy models in male, but not female mice. These data demonstrate the importance of microglial lipid droplets in tau accumulation and reveal REV-ERBα as a therapeutically accessible, sex-dependent regulator of microglial inflammatory signaling, lipid metabolism, and tauopathy.

2023-07-12 | GSE236875 | GEO

Targeting MYC induces lipid droplet accumulation by upregulation of HILPDA in clear cell renal cell carcinoma

Project description:Metabolic reprogramming is critical during clear cell renal cell carcinoma (ccRCC) tumorigenesis, manifested by accumulation of lipid droplets (LDs), organelles that have emerged as new hallmarks of cancer. Yet, regulation of their biogenesis is still poorly understood. Here, we demonstrate that MYC inhibition in ccRCC cells lacking the von Hippel Lindau (VHL) gene leads to increased triglyceride content potentiating LD formation in a glutamine-dependent manner. Notably, LD accumulation is prevented, and tumor burden reduced in vivo upon concurrent inhibition of MYC signaling and glutamine metabolism. Furthermore, we identified the hypoxia inducible lipid droplet associated protein (HILPDA) as the key driver for induction of MYC-driven LD accumulation and demonstrated that conversely, proliferation, LD formation, and tumor growth are impaired upon its downregulation. Finally, analysis of ccRCC tissue as well as healthy renal control samples, postulated HILPDA as a specific ccRCC biomarker. Together, these discoveries provide an attractive approach for development of new therapeutic interventions for the treatment of this type of renal cancer.

2024-01-27 | GSE223069 | GEO

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082R-38_MASTER]

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082R-38_MASTER]

| PRJNA1100201 | ENA

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082-12_MASTER]

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082-12_MASTER]

| PRJNA1100204 | ENA

Analysis of gene expression changes in lipid droplet formation of human liver cancer cell HepG2

Project description:Fatty liver is a condition of excessive triglyceride accumulation in hepatocytes. Additionally, hepatocytes showed a high degree of fat droplet accumulation during excessive alcohol consumption and metabolic syndrome. However, the molecular mechanisms involved in fat droplet formation remain unknown. This study used an in vitro fatty liver formation model of the human liver cancer cell line HepG2 to comprehensively search for fat droplet formation-related genes whose expression changes during fat droplet formation. Microarray analysis with extracted total RNA determined the genes that are involved in fat droplet formation and confirmed their expression by real-time polymerase chain reaction after culturing HepG2 cells in a culture medium containing 0, 50, 200, and 500 μM of oleic acid for 24 h. The results revealed 142 genes demonstrating increased expressions by >2.0 fold with oleic acid treatment and 426 genes demonstrating decreased expressions. Perilipin 2 (PLIN2) was estimated as the gene most closely associated with fatty liver. Lipid droplet formation in HepG2 upregulated PLIN2 in an oleic acid-treated concentration-dependent manner. These results indicate the involvement of genes in oleate treatment-induced lipid droplet formation in HepG2, particularly PLIN2 may play an important role.

2023-12-01 | GSE248166 | GEO

Microglial REV-ERBα regulates inflammation and lipid droplet formation to drive tauopathy

Project description:Alzheimer’s disease is associated with disrupted circadian rhythms and clock gene expression. REV-ERBα (Nr1d1) is a circadian transcriptional repressor involved in the regulation of lipid metabolism and macrophage function. While global REV-ERBα deletion increases microglial activation and mitigates amyloid plaque formation, the cell-autonomous effects of microglial REV-ERBα deletion in healthy brain and in tauopathy are unexplored. Here, we show that microglial REV-ERBα deficient enhances inflammatory signaling, disrupts lipid metabolism, and causes lipid droplet (LD) accumulation specifically in male microglia. Inflammation and LD accumulation combine to inhibit microglial tau phagocytosis, which can be partially rescued by blockage of lipid droplet formation. Microglial REV-ERBα deletion exacerbates tau aggregation and neuroinflammation in P301S and AAV-P301L tauopathy models in male, but not female mice. These data demonstrate the importance of microglial lipid droplets in tau accumulation and reveal REV-ERBα as a therapeutically accessible, sex-dependent regulator of microglial inflammatory signaling, lipid metabolism, and tauopathy.

2023-08-09 | PXD043877 | Pride

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of aged mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-10-30 | GSE139542 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data