Abstract 3805: Furanodienone downregulates EGFR and Her-2 signaling in BT-474 breast cancer cells

• Published in: Cancer research (Chicago, Ill.) Vol. 70; no. 8_Supplement; p. 3805
• Main Authors: Li, Yingwei, Zhu, Guoyuan, Dong, Suisui, Shen, Xiaoling, Yu, Zhiling, Fong, Wang-fun David
• Format: Journal Article
• Language: English
• Published: 15.04.2010
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM10-3805

Abstract Epidermal growth factor receptor (EGFR) and Her-2 are members of the ErbB receptor family of type 1 tyrosine kinases. Also, ligand-induced EGFR /Her-2 heterodimerization triggers potent proliferative and survival signals. EGFR and Her2 frequently overexpress in breast cancer and their overexpression is correlated with a poor prognosis. Therefore dual EGFR/ Her-2 inhibition is an attractive therapeutic strategy for breast cancer treatment. Furanodienone is a compound isolated from Rhizoma Curcumae, which is commonly used in cancer treatment in China. In this study, we used the breast cancer cell BT-474 as the model to investigate the mechanism of furanodienone in breast cancer treatment. We found that furanodienone induced G1 arrest and effectively blocked EGF-stimulated cell cycle progression in BT-474 cells. Moreover, furanodienone decreased protein levels of EGFR, phosphorylation of EGFR and Her-2, so that it prevented the activation of downstream molecules like Akt, Gsk3β and c-Raf, which resulted in inhibiting cell cycle progression. These findings suggested that furanodienone induced growth inhibition in BT-474 human breast cancer cells through inhibiting EGFR /Her-2 signaling pathway. Furthermore, furanodienone and its related compounds provided insights into novel approaches for the prevention and treatment of human breast cancers, especially for those with EGFR /Her-2 overexpression. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3805.