Expression data from murine adipose tissue endothelial cells during pre-cachexia
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ABSTRACT:
PROVIDER: PRJNA875958 | ENA |
REPOSITORIES: ENA
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Project description:Endothelial cells form a barrier between the contents of the blood and adipocytes. We hypothesized that during cancer cachexia development, transcriptomic changes alter angiocrine signals to contribute to adipose tissue remodelling. We used microarrays to observe changes in gene expression in endothelial cells isolated from subcutaneous fat of mice during pre-cachexia.
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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.
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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.
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Project description:Microbiome in murine cancer cachexia
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Project description: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.
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Project description:Cancer cachexia is a multifactorial, largely irreversible metabolic disorder characterized by skeletal muscle and adipose tissue depletion that is responsible for 20% of cancer-related deaths. Oxaliplatin, a platinum-based chemotherapeutic, is a common, first-line treatment for metastatic colorectal and other malignancies that result in cancer cachexia. Yet, it is unknown whether oxaliplatin contributes to these effects independently of cancer. To reveal its role in cachexia development, we administered a chronic human-equivalent oxaliplatin dose to non-tumor-bearing C57BL/6 mice. Daily activity, muscle wasting, fat depletion, and metabolic parameters were monitored through metabolic cages and echo-MRI measurements followed by postmortem muscle and fat tissue histology and bulk RNA seq. Our results show that a high accumulative oxaliplatin dose of 80 mg/kg leads to cachexia-like symptoms, characterized by severe loss of body mass, decreased food intake, diminished ambulatory activity accompanied by lowered core body temperature, decreased skeletal muscle mass, and loss of adipose tissue. RNA-seq data from muscle and adipose tissues indicate a complex mechanism that is in part driven by inflammation and adipokine activity. Comparison of oxaliplatin treatment with external human and murine datasets in cancer and fasting settings illustrates that while oxaliplatin shares many differentially expressed genes with these conditions, it also induces unique gene differentiation. These results suggested oxaliplatin alone induces a cachexia phenotype and thus may aggravate cancer-induced cachexia, highlighting the importance of early diagnostic and therapeutic interventions that target cachexia from both cancer and chemotherapy.
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Project description:Cancer-associated cachexia (CAC) is a multifactorial, metabolic wasting syndrome that coincides with cancer malignancies of multiple entities. CAC is characterized by progressive loss of muscle mass and adipose tissue and diminishes therapy responsiveness. Here, we show that the expression of FGF21 is induced in livers of tumor-bearing mice with CAC. FGF21 deficiency promotes weight loss, exacerbates adipose tissue wasting and increases systemic inflammation, pointing towards a protective role of FGF21 in CAC. In line, IL6-mediated STAT3 activation induces FGF21 expression in hepatocytes as well as adipocytes. FGF21 promotes anabolic signaling cascades, increases cellular glucose uptake in response to IL6 exposure and counteracts cytokine-mediated glycerol release, thereby opposing adipose tissue loss in CAC. Eventually, we find that FGF21 is increased in cancer patients with clinical CAC. Together, we reveal a protective role for FGF21 in experimental CAC and identify the protein as a potential biomarker in clinical cachexia.
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