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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells

  • You, Daeun (Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University) ;
  • Jung, Seung Pil (Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine) ;
  • Jeong, Yisun (Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University) ;
  • Bae, Soo Youn (Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine) ;
  • Lee, Jeong Eon (Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University) ;
  • Kim, Sangmin (Breast Cancer Center, Samsung Medical Center)
  • Received : 2017.06.09
  • Accepted : 2017.08.30
  • Published : 2017.12.31
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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.

Keywords

References

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