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Adipocyte. 2019 Dec;8(1):31-45. doi: 10.1080/21623945.2018.1551688. Epub 2018 Dec 11.

Breast cancer-released exosomes trigger cancer-associated cachexia to promote tumor progression.

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a Department of Breast and Thyroid Surgery , Renmin Hospital of Wuhan University , Wuhan , Hubei , P. R. China.
b Department of Clinical Laboratory , Renmin Hospital of Wuhan University , Wuhan , Hubei , P. R. China.
c Department of Pathology , Renmin Hospital of Wuhan University , Wuhan , Hubei , P. R. China.
d Department of Pathophysiology , Wuhan University School of Basic Medical Sciences , Wuhan , Hubei Province , P. R. China.


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 PPARγ. 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 PPARγ expression, but does not significantly affect biological conversion in C2C12. Likewise, propranolol ameliorates tumour exosomes-associated cachectic wasting through upregulating the PPARγ 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.


Breast cancer; cachexia; exosomes; tumour progression

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