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GPR120 is not required for ω‐3 PUFAs‐induced cell growth inhibition and apoptosis in breast cancer cells
Author(s) -
Zhu Shenglong,
Jiang Xiaowei,
Jiang Siyuan,
Lin Guangxiao,
Gong Jianping,
Chen Wei,
He Zhao,
Chen Yong Q
Publication year - 2018
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10883
Subject(s) - gpr120 , apoptosis , breast cancer , cell growth , cancer research , polyunsaturated fatty acid , carcinogenesis , receptor , cell , biology , medicine , endocrinology , microbiology and biotechnology , cancer , biochemistry , g protein coupled receptor , fatty acid
Intake of ω‐3 PUFAs reduces the frequency of breast cancer, and GPR120 receptor transduces ω‐3 PUFAs signaling to increase insulin sensitivity in mice, but whether GPR120 mediates ω‐3 PUFAs signaling to inhibit breast carcinogenesis is currently unknown. In the present study, we found that GPR120 is highly expressed in human breast cancerous tissues but not adjacent normal tissue. Knockdown of GPR120 by siRNA in breast cancer cells significantly reduced cell growth, and dramatically increased ω‐3 FFA‐induced cell growth inhibition and apoptosis. Thus, these observations indicated that GPR120 promotes breast cancer cell growth, whereas ω‐3 PUFA‐induce breast cancer cell apoptosis independently of GPR120.