Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells

BMB Reports

Yisun Jeong^1¹  Daeun You^1²  Seung Pil Jung^4³  Soo Youn Bae^4⁴ 

[1]Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea^3

[2]Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea^1

[3]Departments of Surgery, Samsung Medical Center, Seoul 06351, Korea^2

[4]Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea^4

关键词: Akt pathway;   

DOI  :  10.5483/BMBRep.2017.50.12.096

学科分类：生物化学/生物物理

来源: Korean Society for Biochemistry and Molecular Biology

【 摘 要 】

Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients with luminal type A breast cancer. In addition, FN was upregulated in TamR cells. To investigate the mechanism by which FN expression is regulated, we assessed the levels of phosphorylated Akt, JNK, and STAT3 and found that they were all increased in TamR cells. Induction of FN expression was dampened by LY294002 or AKT IV in TamR cells. Furthermore, FN expression was increased by constitutively active (CA)-Akt overexpression in tamoxifen-sensitive MCF7 (TamS) cells and colony formation of TamR cells was blocked by AKT IV treatment. Taken together, these results demonstrate that FN expression is upregulated through the PI-3K/Akt pathway in tamoxifen-resistant breast cancer cells.

【 授权许可】

Unknown