CD36
脂肪细胞
癌症研究
脂肪生成
脂肪酸
脂质代谢
肿瘤微环境
癌细胞
生物
脂肪组织
化学
上皮-间质转换
脂肪酸合成
癌症
细胞生物学
内分泌学
生物化学
转移
受体
肿瘤细胞
遗传学
作者
Jones Gyamfi,Joo Hye Yeo,DoYong Kwon,Byung Soh Min,Yoon Jin,Ja Seung Koo,Joon Jeong,Jinu Lee,Jong Myung Choi
标识
DOI:10.1038/s41523-021-00324-7
摘要
Abstract Adipocytes influence breast cancer behaviour via fatty acid release into the tumour microenvironment. Co-culturing human adipocytes and breast cancer cells increased CD36 expression, with fatty acid import into breast cancer cells. Genetic ablation of CD36 attenuates adipocyte-induced epithelial-mesenchymal transition (EMT) and stemness. We show a feedforward loop between CD36 and STAT3; where CD36 activates STAT3 signalling and STAT3 binds to the CD36 promoter, regulating its expression. CD36 expression results in metabolic reprogramming, with a shift towards fatty acid oxidation. CD36 inhibition induces de novo lipogenesis in breast cancer cells. Increased CD36 expression occurs with increased FABP4 expression. We showed that CD36 directly interacts with FABP4 to regulate fatty acid import, transport, and metabolism. CD36 and FABP4 inhibition induces apoptosis in tumour cells. These results indicate that CD36 mediates fatty acid import from adipocytes into cancer cells and activates signalling pathways that drive tumour progression. Targeting CD36 may have a potential for therapy, which will target the tumour microenvironment.
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