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Breast Cancer Research

Open Access

HER2 upregulates fatty acid synthase and acetyl-CoA carboxylase at a translational level in breast cancer cells

  • S Yoon1, 2,
  • M-Y Lee1, 2,
  • B-W Park3 and
  • K-S Kim1, 2
Breast Cancer Research20057(Suppl 2):P4.02

https://doi.org/10.1186/bcr1132

Published: 17 June 2005

Keywords

RapamycinmTOR SignalingHuman Breast CarcinomaHER2 OverexpressionmTOR Signaling Pathway

Overexpression of the HER2 oncogene is observed in approximately 30% of human breast carcinoma specimens. HER2-overexpressing breast cancer cells, such as SK-BR-3 and BT-474 cells, express fatty acid synthase (FAS) at a higher level than MCF-7 cells or MDA-MB-231 cells, where HER2 is expressed at a moderate or low level. Adenovirus-mediated HER2 expression in MDA-MB-231 cells increased acetyl-CoA carboxylase alpha (ACCα) and FAS protein levels without significant increases of their mRNA. HER2-mediated increases of ACCα and FAS proteins were inhibited by the PI3K inhibitor, LY294002, and the mTOR inhibitor, rapamycin. But sterol regulatory element-binding protein 1 (SREBP1) and ATP citrate lyase (ACL) mRNA and protein levels were not changed by HER2 overexpression, LY294002 or rapamycin. In conclusion, our results suggest that HER2-overexpressing cells lead to increased ACCα and FAS proteins at a translational level via the activation of the mTOR signaling pathway and not through SREBP-1c-mediated transcriptional activation.

Authors’ Affiliations

(1)
Department of Biochemistry and Molecular Biology, BK21 Project, Yonsei University, College of Medicine, Seoul, Korea
(2)
Center for Chronic Metabolic Disease Research, BK21 Project, Yonsei University, College of Medicine, Seoul, Korea
(3)
Department of Surgery, BK21 Project, Yonsei University, College of Medicine, Seoul, Korea

Copyright

© BioMed Central 2005

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