Down-regulation of fatty acid synthase is associated with decreased Akt activation in lovastatin induced apoptosis cells

Yuan Ching Chang, Yen Hua Huang, Chwen Ming Shih, Jui Yu Wu, Chien Liang Liu, Shwu Huey Wang, Chun Mao Lin

研究成果: 雜誌貢獻文章

2 引文 (Scopus)

摘要

Increased fatty acid synthase (FAS) protein expression is coordinated with cancer development. FAS inhibitors become a focus of anticancer drug development. Lovastatin, one of the active ingredients in red yeast rice, is a product of Monascus purpureus. Lovastatin has been shown to inhibit proliferation and to induce apoptosis in a variety of tumor cells. This report shows that chemopreventive effects of lovastatin may be through the down regulation of FAS. Lovastatin exhibited significant apoptosis-inducing activity in HL-60 cells, as observed by flow cytometry (with 49.83% in sub-GI peak compared to the control, 10.43%), blebbing cell membrane morphology, and nuclear condensation. Cellular triglyceride, cholesterol, and free fatty acid in HepG2 cells were reduced to 79%, 81%, and 75%, respectively, upon lovastatin treatment (50 μM) for 4 h. The relative levels of FAS protein after treatment with 0, 10, 20, and 50 μM lovastatin were 1.00, 0.89, 0.72, and 0.31, respectively. Phosphorylated Akt was reduced in a dose-dependent manner. Reverse transcription PCR analysis showed that lovastatin upregulated PPAR-γ and inhibited SREBP-1 mRNA expression in HepG2 cells. Our current results implicate that lovastatin inhibiting FAS expression is associated with the decreased Akt activation.

原文英語
頁(從 - 到)340-345
頁數6
期刊Journal of Food and Drug Analysis
14
發行號4
出版狀態已發佈 - 十二月 2006

指紋

lovastatin
Lovastatin
Fatty Acid Synthases
fatty-acid synthase
Down-Regulation
apoptosis
Apoptosis
cells
Hep G2 Cells
red yeast rice
Monascus
Monascus purpureus
Peroxisome Proliferator-Activated Receptors
antineoplastic agents
HL-60 Cells
Blister
active ingredients
Nonesterified Fatty Acids
Reverse Transcription
flow cytometry

ASJC Scopus subject areas

  • Food Science
  • Pharmacology

引用此文

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title = "Down-regulation of fatty acid synthase is associated with decreased Akt activation in lovastatin induced apoptosis cells",
abstract = "Increased fatty acid synthase (FAS) protein expression is coordinated with cancer development. FAS inhibitors become a focus of anticancer drug development. Lovastatin, one of the active ingredients in red yeast rice, is a product of Monascus purpureus. Lovastatin has been shown to inhibit proliferation and to induce apoptosis in a variety of tumor cells. This report shows that chemopreventive effects of lovastatin may be through the down regulation of FAS. Lovastatin exhibited significant apoptosis-inducing activity in HL-60 cells, as observed by flow cytometry (with 49.83{\%} in sub-GI peak compared to the control, 10.43{\%}), blebbing cell membrane morphology, and nuclear condensation. Cellular triglyceride, cholesterol, and free fatty acid in HepG2 cells were reduced to 79{\%}, 81{\%}, and 75{\%}, respectively, upon lovastatin treatment (50 μM) for 4 h. The relative levels of FAS protein after treatment with 0, 10, 20, and 50 μM lovastatin were 1.00, 0.89, 0.72, and 0.31, respectively. Phosphorylated Akt was reduced in a dose-dependent manner. Reverse transcription PCR analysis showed that lovastatin upregulated PPAR-γ and inhibited SREBP-1 mRNA expression in HepG2 cells. Our current results implicate that lovastatin inhibiting FAS expression is associated with the decreased Akt activation.",
keywords = "Fatty acid synthase, Lovastatin, PKB/Akt, PPAR, SREBP, Statin",
author = "Chang, {Yuan Ching} and Huang, {Yen Hua} and Shih, {Chwen Ming} and Wu, {Jui Yu} and Liu, {Chien Liang} and Wang, {Shwu Huey} and Lin, {Chun Mao}",
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T1 - Down-regulation of fatty acid synthase is associated with decreased Akt activation in lovastatin induced apoptosis cells

AU - Chang, Yuan Ching

AU - Huang, Yen Hua

AU - Shih, Chwen Ming

AU - Wu, Jui Yu

AU - Liu, Chien Liang

AU - Wang, Shwu Huey

AU - Lin, Chun Mao

PY - 2006/12

Y1 - 2006/12

N2 - Increased fatty acid synthase (FAS) protein expression is coordinated with cancer development. FAS inhibitors become a focus of anticancer drug development. Lovastatin, one of the active ingredients in red yeast rice, is a product of Monascus purpureus. Lovastatin has been shown to inhibit proliferation and to induce apoptosis in a variety of tumor cells. This report shows that chemopreventive effects of lovastatin may be through the down regulation of FAS. Lovastatin exhibited significant apoptosis-inducing activity in HL-60 cells, as observed by flow cytometry (with 49.83% in sub-GI peak compared to the control, 10.43%), blebbing cell membrane morphology, and nuclear condensation. Cellular triglyceride, cholesterol, and free fatty acid in HepG2 cells were reduced to 79%, 81%, and 75%, respectively, upon lovastatin treatment (50 μM) for 4 h. The relative levels of FAS protein after treatment with 0, 10, 20, and 50 μM lovastatin were 1.00, 0.89, 0.72, and 0.31, respectively. Phosphorylated Akt was reduced in a dose-dependent manner. Reverse transcription PCR analysis showed that lovastatin upregulated PPAR-γ and inhibited SREBP-1 mRNA expression in HepG2 cells. Our current results implicate that lovastatin inhibiting FAS expression is associated with the decreased Akt activation.

AB - Increased fatty acid synthase (FAS) protein expression is coordinated with cancer development. FAS inhibitors become a focus of anticancer drug development. Lovastatin, one of the active ingredients in red yeast rice, is a product of Monascus purpureus. Lovastatin has been shown to inhibit proliferation and to induce apoptosis in a variety of tumor cells. This report shows that chemopreventive effects of lovastatin may be through the down regulation of FAS. Lovastatin exhibited significant apoptosis-inducing activity in HL-60 cells, as observed by flow cytometry (with 49.83% in sub-GI peak compared to the control, 10.43%), blebbing cell membrane morphology, and nuclear condensation. Cellular triglyceride, cholesterol, and free fatty acid in HepG2 cells were reduced to 79%, 81%, and 75%, respectively, upon lovastatin treatment (50 μM) for 4 h. The relative levels of FAS protein after treatment with 0, 10, 20, and 50 μM lovastatin were 1.00, 0.89, 0.72, and 0.31, respectively. Phosphorylated Akt was reduced in a dose-dependent manner. Reverse transcription PCR analysis showed that lovastatin upregulated PPAR-γ and inhibited SREBP-1 mRNA expression in HepG2 cells. Our current results implicate that lovastatin inhibiting FAS expression is associated with the decreased Akt activation.

KW - Fatty acid synthase

KW - Lovastatin

KW - PKB/Akt

KW - PPAR

KW - SREBP

KW - Statin

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