The crosstalk: exosomes and lipid metabolism

Wang, Wei; Zhu, Neng; Yan, Tao; Shi, Yaning; Chen, Jing; Zhang, Chanjuan; Xie, Xue-Jiao; Liao, Duan‐Fang; Qin, Li

doi:10.1186/s12964-020-00581-2

Cited by 106 publications

(72 citation statements)

References 130 publications

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“…Leukotriene is an effective pro-inflammatory lipid intermediary. Neutral sphingomyelinase overexpressed in exosomes can catalyze the production of ceramide and lead to neuronal apoptosis ( 30 ). The results of this study showed that the medium of WI-38 cells 24 h after irradiation with 2 Gy of carbon ions significantly inhibited the migration and invasion of A549 cells, which may be that carbon ion radiation bystander changed the metabolic pattern of A549 cells, thereby inhibiting tumor metastasis.…”

Section: Discussionmentioning

confidence: 99%

Effect of Carbon Ion Radiation Induces Bystander Effect on Metastasis of A549 Cells and Metabonomic Correlation Analysis

et al. 2021

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ObjectiveTo analyze the effect of carbon ion (12C6+) radiation may induce bystander effect on A549 cell metastasis and metabonomics.MethodsA549 cell was irradiated with carbon ion to establish the clone survival model and the transwell matrix assay was applied to measure the effect of carbon ion on cell viability, migration, and invasion, respectively. Normal human embryonic lung fibroblasts (WI-38) were irradiated with carbon ions of 0 and 2 Gy and then transferred to A549 cell co-culture medium for 24 h. The migration and invasion of A549 cells were detected by the Transwell chamber. The analysis of metabonomic information in transfer medium by liquid phase mass spectrometry (LC-MS), The differential molecules were obtained by principal pomponent analysis (PCA) and the target proteins of significant differences (p = 1.7 × 10−3) obtained by combining with the STICH database. KEGG pathway was used to analyze the enrichment of the target protein pathway.ResultsCompared with 0 Gy, the colony formation, migration, and invasion of A549 cells were significantly inhibited by carbon ion 2 and 4 Gy irradiation, while the inhibitory effect was not significant after 1 Gy irradiation. Compared with 0 Gy, the culture medium 24 h after carbon ion 2 Gy irradiation significantly inhibited the metastasis of tumor cells (p = 0.03). LC-MS analysis showed that 23 differential metabolites were obtained in the cell culture medium 24 h after carbon ion 0 and 2 Gy irradiation (9 up-regulated and 14 down-regulated). Among them, two were up-regulated and two down-regulated (p = 2.9 × 10−3). 41 target proteins were corresponding to these four differential molecules. Through the analysis of the KEGG signal pathway, it was found that these target molecules were mainly enriched in purine metabolism, tyrosine metabolism, cysteine and methionine metabolism, peroxisome, and carbon metabolism. Neuroactive ligand-receptor interaction, calcium signaling pathway, arachidonic acid metabolism, and Fc epsilon RI signaling pathway.ConclusionThe bystander effect induced by 2 Gy carbon ion radiation inhibits the metastasis of tumor cells, which indicates that carbon ions may change the metabolites of irradiated cells, so that it may indirectly affect the metabolism of tumor cell growth microenvironment, thus inhibiting the metastasis of malignant tumor cells.

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Section: Discussionmentioning

confidence: 99%

Effect of Carbon Ion Radiation Induces Bystander Effect on Metastasis of A549 Cells and Metabonomic Correlation Analysis

et al. 2021

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“…which may cause, among other things, metabolic changes [ 131 , 132 , 133 ]. However, a growing number of reports provide evidence that extracellular vesicles can regulate the expression of classical lipid transporters such as CD36, ATP-binding cassette transporter A1 (ABCA1), low-density lipoprotein receptor (LDLR), and ATP-Binding Cassette Subfamily G Member 1 (ABCG1) [ 134 ]. A targeted quantitative lipidomic analysis of EVs and cells derived from high-metastatic (D3H2LN) and low-metastatic (D3H1) TNBC cell lines found that unsaturated diacylglycerol species were upregulated in EVs from high-metastatic D3H2LN cells when compared with low-metastatic D3H1 cells without an increase in secreting cells.…”

Section: Tumor-derived Extracellular Vesicles (Evs) Modulate Breasmentioning

confidence: 99%

Expanding Roles of De Novo Lipogenesis in Breast Cancer

Simeone

Tacconi

Longo

et al. 2021

IJERPH

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In recent years, lipid metabolism has gained greater attention in several diseases including cancer. Dysregulation of fatty acid metabolism is a key component in breast cancer malignant transformation. In particular, de novo lipogenesis provides the substrate required by the proliferating tumor cells to maintain their membrane composition and energetic functions during enhanced growth. However, it appears that not all breast cancer subtypes depend on de novo lipogenesis for fatty acid replenishment. Indeed, while breast cancer luminal subtypes rely on de novo lipogenesis, the basal-like receptor-negative subtype overexpresses genes involved in the utilization of exogenous-derived fatty acids, in the synthesis of triacylglycerols and lipid droplets, and fatty acid oxidation. These metabolic differences are specifically associated with genomic and proteomic changes that can perturb lipogenic enzymes and related pathways. This behavior is further supported by the observation that breast cancer patients can be stratified according to their molecular profiles. Moreover, the discovery that extracellular vesicles act as a vehicle of metabolic enzymes and oncometabolites may provide the opportunity to noninvasively define tumor metabolic signature. Here, we focus on de novo lipogenesis and the specific differences exhibited by breast cancer subtypes and examine the functional contribution of lipogenic enzymes and associated transcription factors in the regulation of tumorigenic processes.

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“…Recently, many studies have focused on the relationship between exosomes and lipid disorder. Exosomes-mediated lipid metabolism covers the process of lipid synthesis, transportation, and degradation, which have been implicated in atherosclerosis 118 . For example, exosomes are an adequately potent source of eicosanoids such as prostaglandins and leukotrienes, both of which are active in vivo and in vitro .…”

Section: Exosomal Changes Related To Atherosclerosis Risk Factorsmentioning

confidence: 99%

“…Furthermore, substantial evidence suggests that brown adipose tissue (BAT)-derived exosomes can alleviate lipid accumulation and improve cardiac function, indicating that exosomes are involved in lipid degradation and adipose tissue redistribution 121 . In turn, growing evidence suggests that lipid metabolism affects the biological functions of exosomes, including bioprocesses from signal transduction by receptor-ligand interactions and exosome internalization by or fusion with recipient cells, which provides a new perspective for better understanding the occurrence and development of atherosclerosis 118 .…”

Section: Exosomal Changes Related To Atherosclerosis Risk Factorsmentioning

confidence: 99%

Exosomes in atherosclerosis: performers, bystanders, biomarkers, and therapeutic targets

Wang

Liu

et al. 2021

Theranostics

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Exosomes are nanosized lipid vesicles originating from the endosomal system that carry many macromolecules from their parental cells and play important roles in intercellular communication. The functions and underlying mechanisms of exosomes in atherosclerosis have recently been intensively studied. In this review, we briefly introduce exosome biology and then focus on advances in the roles of exosomes in atherosclerosis, specifically exosomal changes associated with atherosclerosis, their cellular origins and potential functional cargos, and their detailed impacts on recipient cells. We also discuss the potential of exosomes as biomarkers and drug carriers for managing atherosclerosis.

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The crosstalk: exosomes and lipid metabolism

Cited by 106 publications

References 130 publications

Effect of Carbon Ion Radiation Induces Bystander Effect on Metastasis of A549 Cells and Metabonomic Correlation Analysis

Effect of Carbon Ion Radiation Induces Bystander Effect on Metastasis of A549 Cells and Metabonomic Correlation Analysis

Expanding Roles of De Novo Lipogenesis in Breast Cancer

Exosomes in atherosclerosis: performers, bystanders, biomarkers, and therapeutic targets

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