Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells

Eun Soo Lee; Jung Ok Lee; Soo Kyung Lee; Ji Hae Kim; Jin Hee Jung; Bora Keum; Sun Hwa Park; Hyeon Soo Kim

doi:10.1016/j.lfs.2009.03.004

Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells

Eun Soo Lee, Jung Ok Lee, Soo Kyung Lee, Ji Hae Kim, Jin Hee Jung, Bora Keum, Sun Hwa Park, Hyeon Soo Kim

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

9 Citations (Scopus)

Abstract

Aim: The aim of this study is to characterize the roles of caffeic acid phenethyl ester (CAPE) in the skeletal muscle cells. Main methods: We performed immunoblotting assay using various phosphorylation specific antibodies. Key findings: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3β in a phosphoinositide 3-kinase (PI3K)-dependent manner. CAPE also decreases phosphorylation of β-catenin, ultimately leading to β-catenin accumulation. In addition, we demonstrated that CAPE activated the mammalian target of rapamycin (mTOR)-p70 S6 ribosomal kinase (S6K) and also stimulated extracellular signal-regulated kinase (ERK). The inhibition of mTOR blocked CAPE-induced ERK phosphorylation. Significance: Our results suggest that CAPE may act through β-catenin accumulation via stimulation of GSK-3β and may also participate in cellular proliferation through the mTOR-ERK pathway.

Original language	English
Pages (from-to)	755-759
Number of pages	5
Journal	Life Sciences
Volume	84
Issue number	21-22
DOIs	https://doi.org/10.1016/j.lfs.2009.03.004
Publication status	Published - 2009 May 22

Bibliographical note

Funding Information:
This study was supported by a grant from the Korea University College of Medicine and Korea Science and Engineering Foundation Grant KOSEF, R01-2008-11180-0. We declare no conflicts of interests.

Keywords

Akt
CAPE
GSK-3β
mTOR
β-catenin

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)
Pharmacology, Toxicology and Pharmaceutics(all)

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10.1016/j.lfs.2009.03.004

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title = "Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells",

abstract = "Aim: The aim of this study is to characterize the roles of caffeic acid phenethyl ester (CAPE) in the skeletal muscle cells. Main methods: We performed immunoblotting assay using various phosphorylation specific antibodies. Key findings: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3β in a phosphoinositide 3-kinase (PI3K)-dependent manner. CAPE also decreases phosphorylation of β-catenin, ultimately leading to β-catenin accumulation. In addition, we demonstrated that CAPE activated the mammalian target of rapamycin (mTOR)-p70 S6 ribosomal kinase (S6K) and also stimulated extracellular signal-regulated kinase (ERK). The inhibition of mTOR blocked CAPE-induced ERK phosphorylation. Significance: Our results suggest that CAPE may act through β-catenin accumulation via stimulation of GSK-3β and may also participate in cellular proliferation through the mTOR-ERK pathway.",

keywords = "Akt, CAPE, GSK-3β, mTOR, β-catenin",

author = "Lee, {Eun Soo} and Lee, {Jung Ok} and Lee, {Soo Kyung} and Kim, {Ji Hae} and Jung, {Jin Hee} and Bora Keum and Park, {Sun Hwa} and Kim, {Hyeon Soo}",

note = "Funding Information: This study was supported by a grant from the Korea University College of Medicine and Korea Science and Engineering Foundation Grant KOSEF, R01-2008-11180-0. We declare no conflicts of interests.",

year = "2009",

month = may,

day = "22",

doi = "10.1016/j.lfs.2009.03.004",

language = "English",

volume = "84",

pages = "755--759",

journal = "Life Sciences",

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TY - JOUR

T1 - Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells

AU - Lee, Eun Soo

AU - Lee, Jung Ok

AU - Lee, Soo Kyung

AU - Kim, Ji Hae

AU - Jung, Jin Hee

AU - Keum, Bora

AU - Park, Sun Hwa

AU - Kim, Hyeon Soo

N1 - Funding Information: This study was supported by a grant from the Korea University College of Medicine and Korea Science and Engineering Foundation Grant KOSEF, R01-2008-11180-0. We declare no conflicts of interests.

PY - 2009/5/22

Y1 - 2009/5/22

N2 - Aim: The aim of this study is to characterize the roles of caffeic acid phenethyl ester (CAPE) in the skeletal muscle cells. Main methods: We performed immunoblotting assay using various phosphorylation specific antibodies. Key findings: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3β in a phosphoinositide 3-kinase (PI3K)-dependent manner. CAPE also decreases phosphorylation of β-catenin, ultimately leading to β-catenin accumulation. In addition, we demonstrated that CAPE activated the mammalian target of rapamycin (mTOR)-p70 S6 ribosomal kinase (S6K) and also stimulated extracellular signal-regulated kinase (ERK). The inhibition of mTOR blocked CAPE-induced ERK phosphorylation. Significance: Our results suggest that CAPE may act through β-catenin accumulation via stimulation of GSK-3β and may also participate in cellular proliferation through the mTOR-ERK pathway.

AB - Aim: The aim of this study is to characterize the roles of caffeic acid phenethyl ester (CAPE) in the skeletal muscle cells. Main methods: We performed immunoblotting assay using various phosphorylation specific antibodies. Key findings: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3β in a phosphoinositide 3-kinase (PI3K)-dependent manner. CAPE also decreases phosphorylation of β-catenin, ultimately leading to β-catenin accumulation. In addition, we demonstrated that CAPE activated the mammalian target of rapamycin (mTOR)-p70 S6 ribosomal kinase (S6K) and also stimulated extracellular signal-regulated kinase (ERK). The inhibition of mTOR blocked CAPE-induced ERK phosphorylation. Significance: Our results suggest that CAPE may act through β-catenin accumulation via stimulation of GSK-3β and may also participate in cellular proliferation through the mTOR-ERK pathway.

KW - Akt

KW - CAPE

KW - GSK-3β

KW - mTOR

KW - β-catenin

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Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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