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

doi:10.5483/BMBRep.2017.50.12.096

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 journal › Article › peer-review

16 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 language	English
Pages (from-to)	615-620
Number of pages	6
Journal	BMB reports
Volume	50
Issue number	12
DOIs	https://doi.org/10.5483/BMBRep.2017.50.12.096
Publication status	Published - 2017 Dec 1
Externally published	Yes

Keywords

Akt pathway
Fibronectin
Poor prognosis
Tamoxifen resistance

ASJC Scopus subject areas

Biochemistry
Molecular Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.5483/BMBRep.2017.50.12.096

Cite this

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

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 = "Akt pathway, Fibronectin, Poor prognosis, Tamoxifen resistance",

author = "Daeun You and Jung, {Seung Pil} and Yisun Jeong and Bae, {Soo Youn} and Lee, {Jeong Eon} and Sangmin Kim",

note = "Funding Information: This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), which is funded by the Ministry of Education (2016R1D1A1B01010508) and by the Korea University Grant (K1512621) and by a National Research Foundation of Korea (NRF) Grant funded by the Korean Government (MSIP) (2016R1A5A2945889) Publisher Copyright: {\textcopyright} 2017 by the The Korean Society for Biochemistry and Molecular Biology.",

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doi = "10.5483/BMBRep.2017.50.12.096",

language = "English",

volume = "50",

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T1 - Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells

AU - You, Daeun

AU - Jung, Seung Pil

AU - Jeong, Yisun

AU - Bae, Soo Youn

AU - Lee, Jeong Eon

AU - Kim, Sangmin

N1 - Funding Information: This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), which is funded by the Ministry of Education (2016R1D1A1B01010508) and by the Korea University Grant (K1512621) and by a National Research Foundation of Korea (NRF) Grant funded by the Korean Government (MSIP) (2016R1A5A2945889) Publisher Copyright: © 2017 by the The Korean Society for Biochemistry and Molecular Biology.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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.

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KW - Fibronectin

KW - Poor prognosis

KW - Tamoxifen resistance

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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