Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Otopetrin 1 in white adipose predicts the progression of cancer cachexia and protects against weight loss

ABSTRACT: Cancer cachexia is a major cause of mortality in cancer patients, and white adipose tissue (WAT) remodeling precedes weight loss. This study aimed to identify key genes driving cachexia progression and to target WAT loss for early intervention. Using Lewis lung carcinoma mouse models of pre-cachexia and cachexia, we systematically analyzed transcriptomic alterations in pathways and gene expression in WAT. Otopetrin 1 (OTOP1) was identified as a critical regulator of metabolic remodeling and inflammation. Overexpression of OTOP1 in adipocytes induced by tumor-conditioned medium attenuated lipolysis, promoted lipogenesis and exerted anti-inflammatory effects by inhibiting NF-κB signaling and activating PPARγ. In patients with cancer, OTOP1 expression in subcutaneous WAT was markedly reduced in cachexia and was associated with decreased BMI, albumin and hemoglobin, reflecting nutritional deterioration. Collectively, these findings demonstrate that OTOP1 regulates adipose metabolism and inflammation and may serve as a potential biomarker and therapeutic target for cancer cachexia.

ORGANISM(S): Mus musculus

PROVIDER: GSE317738 | GEO | 2026/05/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Differentially expressed lncRNAs and mRNAs in the adipose tissue between cancer associated cachexia mice and normal mice

Project description:Cancer associated cachexia (CAC) causes white adipose tissue (WAT) lose by inhibiting adipogenesis, and promoting lipolysis, fat oxidation and browning. To uncover the specific lncRNAs and mRNAs involved in these processes, we used RNA microarray to identify the transcriptomes and found numerous lncRNAs and mRNAs differentially expressed in the fat tissue between CAC and normal mice.

2018-08-16 | GSE118611 | GEO

ADIPOSE TISSUE PATHWAYS INVOLVED IN WEIGHT LOSS OF CANCER CACHEXIA

Project description:The regulatory gene pathways underlying the loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling. Gene expression profiles (Human Gene 1.0 ST) of abdominal subcutaneous adipose tissue were studied in gastrointestinal cancer patients with (N=13) or without (N=14) cachexia. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.

2010-04-10 | E-GEOD-20571 | biostudies-arrayexpress

ADIPOSE TISSUE PATHWAYS INVOLVED IN WEIGHT LOSS OF CANCER CACHEXIA

Project description:The regulatory gene pathways underlying the loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling.

2010-04-10 | GSE20571 | GEO

Tumor-derived exosomal miR-204 enhances white adipose tissue browning to promote cancer associated cachexia

Project description:Cachexia is a wasting disorder of adipose tissues that leads to profound weight loss and frailty. One key characteristic of cachexia is elevated resting energy expenditure, which has been linked to increased fat lipolysis and thermogenesis. Extracellular vesicles (EVs) are serving as new messengers to mediate cell-cell communication in vivo. How tumors induce brown fat activity is unknown. Here, we found that breast cancer increased hypoxia inducible factor 1 subunit alpha (HIF1A) protein modification through extracellular-vesicle-encapsulated miR-204 targeting von Hippel-Lindau tumor suppressor (VHL), plays an important role in wasting by driving lipolysis and thermogenic gene expression in adipose tissues.

2023-07-13 | GSE222380 | GEO

Cancer-cell-secreted miR-204-5p induces leptin signaling pathway in white adipose tissue to promote cancer-associated cachexia

2024-07-23 | GSE239524 | GEO

Development of a peptide drug restoring AMPK and adipose tissue functionality in cancer cachexia

Project description:Cancer cachexia is a severe systemic wasting disease that negatively affects quality of life and survival in patients with cancer. To date, treating cancer cachexia is still a major unmet clinical need. We recently discovered the destabilization of the AMPK complex in adipose tissue as a key event in cachexia-related adipose tissue dysfunction and developed an AAV-based approach to prevent AMPK degradation and prolong cachexia-free survival. Here, we show the development and optimization of a prototypic peptide, Pen-X-ACIP, where the AMPK stabilizing peptide ACIP is fused to the cell-penetrating peptide moiety penetratin via a propargylic glycine linker to enable late-stage functionalization using click chemistry. Pen-X-ACIP was efficiently taken up by adipocytes, inhibited lipolysis and restored AMPK signaling. Tissue uptake assays showed a favorable uptake profile into adipose tissue upon intraperitoneal injection. Systemic delivery of Pen-X-ACIP into tumor-bearing animals prevented the progression of cancer cachexia without affecting tumor growth, and preserved body weight and adipose tissue mass with no discernable side effects in other peripheral organs, thereby achieving proof-of-concept. As Pen-X-ACIP also exerted its anti-lipolytic activity in human adipocytes, it now provides a promising platform for further (pre)clinical development towards a novel, first-in-class approach against cancer cachexia.

2023-07-02 | GSE235940 | GEO

Skeletal muscle transcriptome profile in LLC mice model of cancer cachexia.

Project description:Cancer cachexia is a metabolic syndrome with alterations in gene expression profile that consequently lead to skeletal muscle wasting. Here, we used RNA sequencing to analyze the mRNA expression profile in the tibialis anterior muscles of the Lewis lung carcinoma (LLC) model of cancer cachexia.

2020-05-19 | GSE144567 | GEO

Skeletal muscle transcriptome profile in LLC mice model of cancer cachexia [miRNA-seq]

Project description:Cancer cachexia is a metabolic syndrome with alterations in gene expression profile that consequently lead to skeletal muscle wasting. Here, we used RNA sequencing to analyze the microRNA expression profile in the tibialis anterior muscles of the Lewis lung carcinoma (LLC) model of cancer cachexia.

2020-05-19 | GSE145393 | GEO

Epigenetic Targeting of Bromodomain Protein BRD4 Counteracts Cancer Cachexia and Prolongs Survival

Project description:Cancer cachexia is a devastating metabolic syndrome characterized by systemic inflammation and massive muscle and adipose tissue wasting. Although cancer cachexia is responsible for approximately one third of cancer deaths, no effective therapies are available and the underlying mechanisms have not been fully elucidated.We have found that (+)-JQ1 administration protects tumor-bearing mice from body weight loss, muscle and adipose tissue wasting. Remarkably, in C26-tumor bearing mice (+)-JQ1 administration dramatically prolongs survival, without directly affecting tumor growth. By ChIP-seq analyses, we unveil that the BET proteins directly promote the muscle atrophy program during cachexia. Consistently, BET pharmacological blockade prevents the activation of catabolic genes associated with skeletal muscle atrophy and decreases IL6 systemic levels. Overall, these findings indicate that BET may represent a promising therapeutic target in the management of cancer cachexia.

2017-10-01 | GSE104155 | GEO

Comparison of mRNA expression in white adipose tissue from LLC tumor-bearing mice and controls

Project description:Cancer-associated cachexia (CAC) is a wasting syndrome caused by malignant tumors. Fat loss plays a significant role in the pathophysiology of cancer-associated cachexia. The mechanism of fat loss in CAC includes enhancement of lipolysis, inhibition of lipogenesis and browning of white adipose tissue. In order to discover potentially functional genes in white adipose tissue of CAC, we used transcriptome sequencing technology to find research-valuable genes in white adipose tissue (WAT) of CAC rodent model. C57/bl6 mice with LLC tumors were used as the in vivo model for CAC, while normal mice subcutaneously injected with phosphate buffer solution were used as the control group. Overall, our data revealed genes that were differentially expressed in the white adipose tissue of LLC tumor-bearing mice, providing a molecular framework for the investigation into CAC fat loss.

2023-09-15 | GSE242812 | 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