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^*

^*Corresponding author for this work

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

11 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

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry,Genetics and Molecular Biology

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10.1016/j.lfs.2009.03.004

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@article{422a4f66bcf246b6aa1b008c32ded152,

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",

issn = "0024-3205",

publisher = "Elsevier Inc.",

number = "21-22",

}

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

UR - https://www.scopus.com/pages/publications/67349284717

U2 - 10.1016/j.lfs.2009.03.004

DO - 10.1016/j.lfs.2009.03.004

M3 - Article

C2 - 19303025

AN - SCOPUS:67349284717

SN - 0024-3205

VL - 84

SP - 755

EP - 759

JO - Life Sciences

JF - Life Sciences

IS - 21-22

ER -

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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