Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of mouse lung cancer cell-line tumors grown subcutaneously in adult male C57BL/6 mice with and without high-fat diet-induced obesity

ABSTRACT: Obesity affects the progress of lung cancer. To understand this more, we performed single-cell RNA sequencing of dissociated tumors of four mouse lung cancer cell-lines grown subcutaneously in adult male C57BL/6 mice with and without high-fat diet-induced obesity.

ORGANISM(S): Mus musculus

PROVIDER: GSE280717 | GEO | 2025/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profile at single cell level of mouse lung cancer cell-line tumors grown subcutaneously in adult male C57BL/6 mice with and without high-fat diet-induced obesity

Project description:Gene expression profile at single cell level of mouse lung cancer cell-line tumors grown subcutaneously in adult male C57BL/6 mice with and without high-fat diet-induced obesity

| PRJNA1180094 | ENA

TMT-proteomics of sorted MC38+ tumor cells with high-fat diet

Project description:Obesity is a major cancer risk factor, but the underlying molecular mechanisms are not always known. In this study, we look at proteome remodeling in cancer cells with obesity, comparing tumor cells sorted from mice fed high-fat versus control diet. We conducted 10-plex TMT-proteomics on GFP+ MC38 colorectal adenocarcinoma tumor cells, sorted from subcutaneously implanted tumors 12 days after implantation. This study reveals molecular pathways that change in cancer cells with obesity that promote tumor growth.

2020-12-16 | PXD019495 | Pride

Gene expression profile at single cell level of lungs of adult male and female C57BL/6 mice with andwithout high-fat diet-induced obesity

Project description:Obesity is associated with various lung pathologies. We performed single nucleus RNA sequencing of formalin-fixed lungs of mice to obtain insights on this.

2024-12-31 | GSE279918 | GEO

Expression signatures of long non-coding RNAs and mRNAs in lung tissues in obesity and obesity-related acute lung injury

Project description:This result is expected to identify several lncRNAs and mRNAs that are dysregulated in the lung due to obesity, as well as obesity-associated lncRNAs and mRNAs that are further altered in acute lung injury, as biomarkers specific to obesity-associated acute lung injury. To provide useful information for elucidating the development of acute lung injury exacerbated by obesity and exploring potential therapeutic targets

2024-01-30 | GSE229262 | GEO

Transcript Profiling of High Fat Diet induced Obesity-prone and Obesity-resistant Rats

Project description:Rodents respond to chronic high fat diet in at least two ways: some of them may readily gain body weight and become obese (termed obesity-prone), and others may not (termed obesity-resistant). An integrated approach of transcript and metabolic profiling of obesity-prone and obesity-resistant rats has been conducted, showing significantly different transcript and metabolic profiles in the two phenotypes. The major transcriptional differences involved hepatic fatty acid metabolism and ketogenesis in response to 16 weeks of high fat diet. At the same time, the different metabolic profiles (in liver tissue extracts, serum, and urine) between the two phenotypes could be ascribed to the corresponding pathways identified with multivariate statistical analysis, including fatty acid metabolism, Krebs cycle, and amino acid metabolism. The integration of results from both transcript and metabolic profiling revealed the different responses to dietary intervention of the two phenotypes and the physiological basis of susceptibility to metabolic disease in obesity-prone rats from a systematic view.

2008-05-20 | GSE11492 | GEO

Vascular rarefaction mediates whitening of brown fat in obesity

Project description:Brown adipose tissue (BAT) is a highly vascularized organ with abundant mitochondria that produce heat through uncoupled respiration. Obesity is associated with a reduction of BAT function; however, it is unknown how obesity promotes dysfunctional BAT. Here, using a murine model of diet-induced obesity, we determined that obesity causes capillary rarefaction and functional hypoxia in BAT, leading to a BAT “whitening” phenotype that is characterized by mitochondrial dysfunction, lipid droplet accumulation, and decreased expression of Vegfa. Targeted deletion of Vegfa in adipose tissue of nonobese mice resulted in BAT whitening, supporting a role for decreased vascularity in obesity-associated BAT. Conversely, introduction of VEGF-A specifically into BAT of obese mice restored vascularity, ameliorated brown adipocyte dysfunction, and improved insulin sensitivity. The capillary rarefaction in BAT that was brought about by obesity or Vegfa ablation diminished β-adrenergic signaling, increased mitochondrial ROS production, and promoted mitophagy. These data indicate that overnutrition leads to the development of a hypoxic state in BAT, causing it to whiten through mitochondrial dysfunction and loss. Furthermore, these results link obesity-associated BAT whitening to impaired systemic glucose metabolism.

2024-12-18 | GSE221854 | GEO

Role of small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice.

Project description:Obesity and insulin resistance are two major risk factors underlying the metabolic syndrome. To gain more insight in the role of the small intestine in the etiology of these metabolic disorders, a microarray study was performed on small intestines (SI) of C57BL/6J mice that were fed a high fat diet mimicking the fatty acid composition of a Western-style human diet. The mice became obese and developed dietary fat-induced glucose intolerance. For gene expression profiling, the small intestines were subdivided in three equal parts along the longitudinal axis. The most pronounced effects of dietary fat were detected in part 2 of the small intestine. The biological processes that were most extensively modulated on a high fat diet were related to lipid metabolism, especially β- and ω-fatty acid oxidation seemed to play an important role, cell cycle and inflammation/immune response. An additional secretome analysis revealed differentially expressed secreted proteins, such as Il18, Ffgf15, Mif, Igfbp3 and Angptl4, which might provoke systemic effects in peripheral organs by influencing their metabolic homeostasis. Furthermore, many of the dietary fat-modulated genes and biological processes in small intestine were previously already associated with obesity and/or insulin resistance. Together, the data of this exploratory study provided various leads for an essential role of the small intestine in development of obesity and/or insulin resistance. Keywords: time course

2008-05-13 | GSE8582 | GEO

Obesity and mouse lung transcriptome

Project description:Effect of obesity on mouse lung transcriptome

| PRJEB57780 | ENA

High-fat feeding rapidly induces obesity and lipid derangements in C57BL/6N mice.

Project description:C57BL/6N (B6N) is becoming the standard background for genetic manipulation of the mouse genome. The B6N, whose genome is very closely related to the reference C57BL/6J genome, is versatile in a wide range of phenotyping and experimental settings and large repositories of B6N ES cells have been developed. Here, we present a series of studies showing the baseline characteristics of B6N fed a high-fat diet (HFD) for up to 12 weeks. We show that HFD-fed B6N mice show increased weight gain, fat mass, and hypercholesterolemia compared to control diet-fed mice. In addition, HFD-fed B6N mice display a rapid onset of lipid accumulation in the liver with both macro- and microvacuolation, which became more severe with increasing duration of HFD. Our results suggest that the B6N mouse strain is a versatile background for studying diet-induced metabolic syndrome and may also represent a model for early nonalcoholic fatty liver disease.

| S-EPMC3685703 | biostudies-literature

Tumor genes regulated in obesity-mediated breast cancer

Project description:We developed a post-menopausal orthotopic ER+ breast cancer model that we used to investigate mechanisms of obesity mediated lung metastases. Obesity altered the immune cell composition and function in the primary tumor microenvironment. To identify tumor-derived genes associated with obesity mediated lung metastases we performed RNASeq on tumors grown in lean vs obese mice. From these results we identified a hepatocyte growth factor (HGF)-c-Met (HGF receptor)-CCL2 loop recruiting metastasis-promoting cells.

2022-12-31 | GSE151866 | 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