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

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 w...

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Published inBMB reports Vol. 50; no. 12; pp. 615 - 620
Main Authors You, Daeun, Jung, Seung Pil, Jeong, Yisun, Bae, Soo Youn, Lee, Jeong Eon, Kim, Sangmin
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society for Biochemistry and Molecular Biology 01.12.2017
생화학분자생물학회
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ISSN1976-6696
1976-670X
DOI10.5483/bmbrep.2017.50.12.096

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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. [BMB Reports 2017; 50(12): 615-620].
AbstractList 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. [BMB Reports 2017; 50(12): 615-620].
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. KCI Citation Count: 5
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.
Author Kim, Sangmin
You, Daeun
Jeong, Yisun
Jung, Seung Pil
Bae, Soo Youn
Lee, Jeong Eon
AuthorAffiliation 2 Departments of Surgery, Samsung Medical Center, Seoul 06351, Korea
1 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea
3 Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea
4 Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea
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Snippet 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...
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SubjectTerms Antineoplastic Agents, Hormonal - chemistry
Antineoplastic Agents, Hormonal - pharmacology
Breast Neoplasms - drug therapy
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Drug Resistance, Neoplasm - drug effects
Female
Fibronectins - biosynthesis
Fibronectins - genetics
Fibronectins - metabolism
Humans
MCF-7 Cells
Phosphatidylinositol 3-Kinases - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Real-Time Polymerase Chain Reaction
Tamoxifen - chemistry
Tamoxifen - pharmacology
Tumor Cells, Cultured
Up-Regulation - drug effects
화학
Title Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells
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