154 179

Cited 0 times in

Interaction between CD36 and FABP4 modulates adipocyte-induced fatty acid import and metabolism in breast cancer

 Jones Gyamfi  ;  Joo Hye Yeo  ;  Doru Kwon  ;  Byung Soh Min  ;  Yoon Jin Cha  ;  Ja Seung Koo  ;  Joon Jeong  ;  Jinu Lee  ;  Junjeong Choi 
 NPJ BREAST CANCER, Vol.7(1) : 129, 2021-09 
Journal Title
Issue Date
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.
Files in This Item:
T202104197.pdf Download
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Koo, Ja Seung(구자승) ORCID logo https://orcid.org/0000-0003-4546-4709
Min, Byung Soh(민병소) ORCID logo https://orcid.org/0000-0003-0180-8565
Jeong, Joon(정준) ORCID logo https://orcid.org/0000-0003-0397-0005
Cha, Yoon Jin(차윤진) ORCID logo https://orcid.org/0000-0002-5967-4064
사서에게 알리기


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.