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Adiponectin receptor (ADIPOR1) signaling ameliorates obesity‐dependent cell cycle entry in MCF7 cells
Author(s) -
Connor Michael,
Theriau Christopher
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1027.6
Subject(s) - adiponectin receptor 1 , adipokine , adiponectin , endocrinology , medicine , leptin , adipose tissue , paracrine signalling , ampk , receptor , biology , chemistry , microbiology and biotechnology , obesity , insulin resistance , protein kinase a , phosphorylation
Adipose tissue produces and secretes hormones, termed adipokines, that have endocrine/paracrine effects on a wide variety of tissues. Two of these adipokines (adiponectin and leptin) have cell cycle effects on breast cancer cells and may underlie the molecular link between obesity and breast cancer. Adiponectin (ADIPO) and leptin (LEP) stoichiometrically antagonize each other in MCF7 cells. Stable 2.6‐fold over expression of ADIPOR1 inhibited LEP‐dependent antagonism of ADIPO in MCF7 cells. This effect of ADIPOR1 was also evident in MCF7 cells exposed to media conditioned by adipocytes from high fat diet fed animals (HFD‐CM). HFD‐CM inhibited AMPK, activated AKT, reduced p27 and ADIPOR1 protein levels in MCF7 cells compared to MCF7 cells exposed to CM from chow diet‐fed animals (CD‐CM). Stable overexpression prevented these HFD‐CM effects suggesting that maintenance of ADIPOR1 signaling may prevent obesity‐dependent breast cancer progression.