Abstract:
:Obesity is a leading risk factor for cancer. However, understanding the crosstalk between adipocytes and tumor cells in vivo, independently of dietary contributions, is a major gap in the field. Here we used a prostate cancer (PCa) mouse model in which the signaling adaptor p62/Sqstm1 is selectively inactivated in adipocytes. p62 loss in adipocytes results in increased osteopontin secretion, which mediates tumor fatty acid oxidation and invasion, leading to aggressive metastatic PCa in vivo. Furthermore, p62 deficiency triggers in adipocytes a general shutdown of energy-utilizing pathways through mTORC1 inhibition, which supports nutrient availability for cancer cells. This reveals a central role of adipocyte's p62 in the symbiotic adipose tissue-tumor collaboration that enables cancer metabolic fitness.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Huang J,Duran A,Reina-Campos M,Valencia T,Castilla EA,Müller TD,Tschöp MH,Moscat J,Diaz-Meco MTdoi
10.1016/j.ccell.2018.03.001subject
Has Abstractpub_date
2018-04-09 00:00:00pages
770-784.e6issue
4eissn
1535-6108issn
1878-3686pii
S1535-6108(18)30069-2journal_volume
33pub_type
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