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

Research output: Contribution to journalArticle

7 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 languageEnglish
Pages (from-to)755-759
Number of pages5
JournalLife Sciences
Volume84
Issue number21-22
DOIs
Publication statusPublished - 2009 May 22

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Glycogen Synthase Kinase 3
Catenins
Sirolimus
Phosphorylation
Extracellular Signal-Regulated MAP Kinases
Phosphotransferases
70-kDa Ribosomal Protein S6 Kinases
1-Phosphatidylinositol 4-Kinase
Phosphatidylinositols
Immunoblotting
Muscle Cells
Muscle
caffeic acid phenethyl ester
Assays
Skeletal Muscle
Cells
Cell Proliferation
Antibodies

Keywords

  • β-catenin
  • Akt
  • CAPE
  • GSK-3β
  • mTOR

ASJC Scopus subject areas

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

Cite this

Caffeic acid phenethyl ester accumulates β-catenin through GSK-3β and participates in proliferation through mTOR in C2C12 cells. / Lee, Eun Soo; Lee, Jung Ok; Lee, Soo Kyung; Kim, Ji Hae; Jung, Jin Hee; Keum, Bora; Park, Sun-Hwa; Kim, Hyeon Soo.

In: Life Sciences, Vol. 84, No. 21-22, 22.05.2009, p. 755-759.

Research output: Contribution to journalArticle

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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.",
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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

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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.

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