Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mechanism of FABP4 promoting medulloblastoma growth

ABSTRACT: Our results showed that FABP4 knockdown inhibits medulloblastoma cell proliferation, migration, and elevates the ROS and MDA levels, resulting in tumor cell apoptosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE283192 | GEO | 2025/11/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mechanism of FABP4 promoting medulloblastoma growth

Project description:Mechanism of FABP4 promoting medulloblastoma growth

| PRJNA1192305 | ENA

FABP4 as a critical mediator in osteoporosis: inhibition strategies and therapeutic potential

Project description:Fatty acid-binding protein 4 (FABP4), a key lipid protein in metabolism and inflammation, has been suggested to be linked to osteoporosis (OP), though direct evidence is scarce. Here, we present the first clear evidence of FABP4's significant role in OP, supported by clinical data and comprehensive in vivo and in vitro experiments. Elevated serum FABP4 in OP patients inversely correlates with bone mineral density (BMD), with similar trends observed in OVX mice. While FABP4 does not influence osteoblast differentiation, it promotes osteoclast formation and bone resorption. The FABP4 inhibitor BMS309403, with an IC50 of 0.89 μM, inhibits osteoclast differentiation by modulating calcium ions and suppressing the Ca2+-Calcineurin-NFATc pathway. Oral BMS309403 increased BMD in OVX mice, albeit less effectively than alendronate, whereas bone-targeted PLGA nanoparticles showed comparable efficacy to alendronate. This research identifies FABP4 as a promising therapeutic target for OP, with significant clinical implications.

2025-04-09 | GSE273951 | GEO

FABP4 deficiency ameliorates alcoholic steatohepatitis in mice

Project description:Fatty acid-binding protein 4 (FABP4) plays an essential role in metabolism and inflammatory. However, the role of FABP4 in alcoholic steatohepatitis (ASH) remains unclear. This study aimed to investigate the function of FABP4 and the underlying mechanisms in the progression of ASH.

2024-04-24 | GSE265758 | GEO

Genome wide expression analysis of FABP4 modulation in urothelial cancer cell UM-UC14 and UM-UC9

Project description:Analysis of gene expression profiling in FABP4 modulation UM-UC14 and Um-UC9 cells. The overall objective was to identify genes regulated by PPARÎ³ signaling pathway in particular FABP4 Total RNA was obtained from FABP4 modulated (either by FABP4 knockdown or rosiglitazone treatment) UM-UC14 or UM-UC9 cells compared to untreated control

2013-09-15 | E-GEOD-47993 | biostudies-arrayexpress

Gene expression of C28/I2 cells with FABP4

Project description:FABP4 has been reported to trigger ADAMTS4 overexpression in chondrocytes. Here we described the transcriptional changes of FABP4-treatment.

2023-06-22 | GSE227483 | GEO

Targeting FABP4 Improves Healthy Aging by Rejuvenating Liver Metabolism

Project description:Introduction: Aging is characterized by progressive metabolic dyshomeostasis that increases morbidity and mortality. Solutions for optimizing healthy aging are challenged by lacking appropriate biomarkers. Moreover, druggable targets to rejuvenate the aging-associated metabolic phenotypes remain unavailable. Methods: Proteomics analysis was performed in a cohort of young and elderly adults. Circulating levels of insulin-like growth factor 1 (IGF-1) and fatty acid binding protein 4 (FABP4) were evaluated by ELISA. FABP4 was silenced in elderly mice by adeno-associated virus. Metabolic activities were measured by metabolic cages. Cognitive function was evaluated by Morris water maze. Glucose and lipid metabolism were evaluated by biochemistry assays with blood samples. RNA-seq in mouse liver was performed for transcriptome analysis. Results: Among 9 aging-sensitive proteins shared by both male and female, FABP4 was identified as a reliable aging biomarker in both human and mouse. Silencing FABP4 in elderly mice significantly rejuvenated the aging-associated decline in metabolic activities. FABP4 knockdown reversed the aging-associated metabolic disorders by promoting degradation of cholesterol and fatty acids, while suppressing gluconeogenesis. Transcriptome analysis revealed a restoration of the pro-aging gene reprogramming towards inflammation and metabolic disorders in the liver after FABP4 knockdown. FABP4 overexpression promoted human LO2 cell senescence. Moreover, administration of an FABP4 inhibitor BMS309403 delivered metabolic benefits in elderly mice. Conclusion: Our findings demonstrate FABP4 as a reliable aging biomarker as well as a practicable target to improve healthy aging in the elderly. Keywords: Aging; Biomarkers; FABP4; Metabolic disorders; Rejuvenation; Senescence.

2025-10-13 | GSE215378 | GEO

Effect of exogenous FABP4 (A-FABP/aP2) with and without palmitic acid on gene expression in RAW264.7 macrophages

Project description:Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4. RAW264.7 macrophages were treated with and without 200 nM recombinant FABP4 in the absence and presence of 0.2 mM palmitic acid.

2015-09-19 | E-GEOD-73173 | biostudies-arrayexpress

Fabp4 is Essential for the Maintenance of Leukemia Stem Cells while Sparing Hematopoietic Stem Cells

Project description:Fatty acid-binding protein 4 (FABP4) plays a crucial role in the uptake, transport, and metabolic regulation of fatty acids. Previous research has found that the abnormal expression of FABP4 is associated with certain cancers, and it may become a new target for tumor therapy. We discovered that a haploinsufficient or absent dosage of Fabp4 does not affect the function of hematopoietic stem cells in mice, but significantly impacts the maintenance of leukemia stem cells (LSC). Our findings indicate that while Fabp4 does not influence the initiation of acute myeloid leukemia (AML) transformed by MLL-AF9 (MA9) in mice, it markedly promotes the progression of AML. A haploinsufficient or absent dosage of Fabp4 significantly extends the survival time of MA9 mice. Our research reveals the key role and mechanism of Fabp4 in MA9-LSC, suggesting that Fabp4 is a potential target for selectively eliminating MLL-rearranged leukemia.

2025-03-23 | GSE278587 | GEO

FABP4-mediated lipid accumulation and lipolysis in tumor associated macrophages promote breast cancer metastasis

Project description:Fatty acid binding protein 4 (FABP4) is known to play important roles in lipid metabolism in multple cell types including in macrophages. In the present study, we used single cell RNA-sequencing in macrophages extracted from either wild-type or mice deficient in FABP4 to further explore the pathways downstream of FABP4 in splenic macrophages.

2025-03-21 | GSE262196 | GEO

Fabp4 is Essential for the Maintenance of Leukemia Stem Cells while Sparing Hematopoietic Stem Cells [bulkRNA-seq]

2025-02-19 | GSE289635 | GEO