Exosomal Secretion of Adipose Tissue during Various Physiological States

Quan, Menchus; Kuang, Shihuan

doi:10.1007/s11095-020-02941-6

Cited by 16 publications

(13 citation statements)

References 115 publications

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“…We suspected that adipocyte-origin exosomes ( 10 ) were conveying signals to tumor cells. TME exosomes ( 11 ) have been implicated in EMT ( 12 ), supporting a rationale to purify exosomes from IS or IR adipocyte conditioned media, challenge MCF7 cultures, and test function on a target set of EMT genes (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Although systemic metabolism of the patient clearly plays a major role in the risk of breast cancer progression ( 34 ), the adipocyte contribution to the local signaling in the TME demands further study. As obesity worsens, adipose tissue develops insulin resistance ( 35 , 36 ), which provoked our overall hypothesis that insulin resistance reprograms exosome payloads ( 10 ). IPA shows gene regulation pathways associated with tumor cell aggressiveness (invasiveness, migration, and angiogenesis) are up-regulated by IR cell–derived exosome payloads compared to those from IS cells.…”

Section: Discussionmentioning

confidence: 99%

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Adipocyte-derived exosomes may promote breast cancer progression in type 2 diabetes

et al. 2021

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Adipocyte-derived exosomes may promote breast cancer progression in type 2 diabetes

et al. 2021

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“…Exosomes play a key role in this communication, linking the diseased and healthy cells [53]. As mentioned above, exosomal crosstalk between adipose tissue and cancer cells may be a significant aspect of tumor progression by reprogramming the surrounding cells [54].…”

Section: Sustaining Proliferative Signalingmentioning

confidence: 99%

Adipose Tissue-Derived Extracellular Vesicles and the Tumor Microenvironment: Revisiting the Hallmarks of Cancer

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Franco

et al. 2021

Cancers

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Extracellular vesicles (EVs) are crucial elements that sustain the communication between tumor cells and their microenvironment, and have emerged as a widespread mechanism of tumor formation and metastasis. In obesity, the adipose tissue becomes hypertrophic and hyperplastic, triggering increased production of pro-inflammatory adipokines, such as tumor necrosis factor α, interleukin 6, interleukin 1, and leptin. Furthermore, obese adipose tissue undergoes dysregulation in the cargo content of the released EVs, resulting in an increased content of pro-inflammatory proteins, fatty acids, and oncogenic microRNAs. These alterations drive obesity-associated inflammatory responses both locally and systemically. After being ignored for a long time, adipose tissues have recently received considerable attention as a major player in tumor microenvironment-linked obesity and cancer. The role of adipose tissue in the establishment and progression of cancer is reinforced by its high plasticity and inflammatory content. Such a relationship may be established by direct contact between adipocytes and cancer cells within the microenvironment or systemically, via EV-mediated cell-to-cell communication. Here, we highlight cues evidencing the influence of adipose tissue-derived EVs on the hallmarks of cancer, which are critical for tumor malignancy.

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“…63 During obesity, the level of exosomes increases by 10-fold and does not return to normal levels after weight loss, suggesting that exosomal secretion profile can be as markers for obesity-related diseases. 64 The pathophysiological mechanism of the onset and progression of obesity includes IR, inflammatory secretome and metabolic disorder. 65 IR represents diminished target tissue (liver, muscle, adipose tissue) sensitivity to insulin.…”

Section: Adipose-derived Exosomesmentioning

confidence: 99%

“…101 The expression of miR-223 was significant in the visceral AT of obese mice and patients than in lean individuals, which was found could modulate macrophage phenotype via TLR4 (Toll-like receptor 4)/FBXW7 (F-box and WD-40 domain protein 7) axis to regulate inflammation. 64 In obese adipocyte exosomes, miR-155 can induce the proinflammatory M1-macrophage phenotype by activating STAT1 and repressing STAT6 expression. 102 The level of miR-34a was upregulated in obesity, which can be leading to adipose inflammation via suppresses M2 macrophage polarisation through its repression of Kruppel-like factor 4 (KLF4).…”

Section: Exosomal Mirnas Mediate Lipid Metabolismmentioning

confidence: 99%