Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose tissue browning in cancer-associated cachexia can be attenuated by inhibition of exosome generation.

Hu W., Ru Z., Xiao W., Xiong Z., Wang C., Yuan C.

Animal Study, published in Biochem Biophys Res Commun (2018) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Biochem Biophys Res Commun (2018)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
30340833
DOI
10.1016/j.bbrc.2018.09.139

Abstract (original English)

Cancer-associated cachexia (CAC) is a disorder characterized by unintended weight loss due to skeletal muscle wasting and adipose tissue loss. Although muscle atrophy in this condition has been well studied, the mechanisms underlying adipose tissue loss, which include browning, have not been investigated in detail. In this respect, though recent studies have shown that exosomes from cancer cells can promote lipolysis, the link between exosomes from cancer cells and CAC has not been clearly established. In this study, we investigate if exosomes from Lewis lung carcinoma (LLC) cells can induce lipolysis in vitro (in 3T3-L1 adipocytes) and in vivo (in LLC tumor-bearing mice). We find that exosomes from LLC cells do induce lipolysis in 3T3-L1 adipocytes and that the white adipose tissues of mice with LLC tumors show clear signs of lipolysis. We also find that this lipolysis can be inhibited using the neutral sphingomyelinase inhibitor GW4869. Our results indicate that GW4869 not only inhibits exosome generation and release from LLC cells, but can also inhibit lipolysis induced by LLC-derived exosomes in 3T3-L1 adipocytes. Furthermore, we also demonstrate that LLC tumor-bearing mice treated with GW4869 did not develop CAC. In summary, our results suggest that inhibiting exosome generation and release can inhibit lipolysis and adipose tissue browning, and may be useful as a novel str

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
3T3-L1 CellsAdipocytesAniline CompoundsAnimalsBenzylidene CompoundsBiological TransportCachexiaCarcinoma, Lewis LungCell DifferentiationCell Proliferation

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