Journal
ADIPOCYTE
Volume 8, Issue 1, Pages 31-45Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21623945.2018.1551688
Keywords
Breast cancer; exosomes; cachexia; tumour progression
Categories
Funding
- National Natural Science Foundation of China (NSFC) [81471781]
- National Major Scientific Instruments and Equipment Development Projects [2012YQ160203]
- NSFC [81302314]
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Cancer-secreted exosomes are emerging mediators of cancer-associated cachexia. Here, we show that miR-155 secreted by breast cancer cells is a potent role on the catabolism of adipocytes and muscle cells through targeting the PPAR gamma. After cocultivated with mature adipocytes or C2C12, tumour cells exhibit an aggressive phenotype via inducing epithelial-mesenchymal transition while breast cancer-derived exosomes increased catabolism and release the metabolites in adipocytes and muscle cells. In adipocytes, cancer cell-secreted miR-155 promotes beige/brown differentiation and remodel metabolism in resident adipocytes by downregulating the PPAR gamma expression, but does not significantly affect biological conversion in C2C12. Likewise, propranolol ameliorates tumour exosomes-associated cachectic wasting through upregulating the PPAR gamma expression. In summary, we have demonstrated that the transfer of miR-155 from exosomes acts as an oncogenic signal reprograming systemic energy metabolism and leading to cancer-associated cachexia in breast cancer.
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