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

Daeun You, Seung Pil Jung, Yisun Jeong, Soo Youn Bae, Jeong Eon Lee, Sangmin Kim

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)615-620
Number of pages6
JournalBMB Reports
Volume50
Issue number12
DOIs
Publication statusPublished - 2017 Dec 1

Keywords

  • Akt pathway
  • Fibronectin
  • Poor prognosis
  • Tamoxifen resistance

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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