Ethanol extracts of fruiting bodies of Antrodia cinnamomea exhibit anti-migration action in human adenocarcinoma CL1-0 cells through the MAPK and PI3K/AKT signaling pathways

Ying Yi Chen, Pei Yu Chou, Yi Chung Chien, Chieh Hsi Wu, Tian Shung Wu, Ming Jyh Sheu

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Cancer metastasis is a primary cause of cancer death. Antrodia cinnamomea (A. cinnamomea), a medicinal mushroom in Taiwan, has been shown antioxidant and anticancer activities. In this study, we first observed that ethanol extract of fruiting bodies of A. cinnamomea (EEAC) exerted a concentration-dependent inhibitory effect on migration and motility of CL1-0 cells in the absence of cytotoxicity. The results of a gelatin zymography assay showed that A. cinnamomea suppressed the activity of matrix metalloproteinase (MMP)-2 and MMP-9 in a concentration-dependent manner. Western blot results demonstrated that treatment with A. cinnamomea decreased the expression of MMP-9 and MMP-2; while the expression of the endogenous inhibitors of these proteins, i.e., tissue inhibitors of MMP (TIMP-1 and TIMP-2) increased. Two major compounds from EEAC codycepin and zhankuic acid A alone and together inhibited MMP-9 and MMP-2 expressions. Further investigation revealed that A. cinnamomea suppressed the phosphorylation of p38, and JNK1/2. A. cinnamomea also suppressed the expressions of PI3K and phosphorylation of AKT. This is the first report confirming the anti-migration activity of this potentially beneficial mushroom against human lung adenocarcinoma CL1-0.

Original languageEnglish
Pages (from-to)768-778
Number of pages11
JournalPhytomedicine
Volume19
Issue number8-9
DOIs
Publication statusPublished - Jun 15 2012
Externally publishedYes

Fingerprint

Antrodia
Phosphatidylinositol 3-Kinases
Adenocarcinoma
Ethanol
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Agaricales
Phosphorylation
Tissue Inhibitor of Metalloproteinases
Tissue Inhibitor of Metalloproteinase-2
Matrix Metalloproteinase 1
Tissue Inhibitor of Metalloproteinase-1
Gelatin
Taiwan
Cause of Death
Neoplasms
Antioxidants
Western Blotting
Neoplasm Metastasis

Keywords

  • Antrodia cinnamomea
  • Chinese herb
  • CL1-0
  • Matrix metalloproteinase
  • Metastasis
  • Mushroom

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Pharmaceutical Science
  • Complementary and alternative medicine
  • Molecular Medicine

Cite this

Ethanol extracts of fruiting bodies of Antrodia cinnamomea exhibit anti-migration action in human adenocarcinoma CL1-0 cells through the MAPK and PI3K/AKT signaling pathways. / Chen, Ying Yi; Chou, Pei Yu; Chien, Yi Chung; Wu, Chieh Hsi; Wu, Tian Shung; Sheu, Ming Jyh.

In: Phytomedicine, Vol. 19, No. 8-9, 15.06.2012, p. 768-778.

Research output: Contribution to journalArticle

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abstract = "Cancer metastasis is a primary cause of cancer death. Antrodia cinnamomea (A. cinnamomea), a medicinal mushroom in Taiwan, has been shown antioxidant and anticancer activities. In this study, we first observed that ethanol extract of fruiting bodies of A. cinnamomea (EEAC) exerted a concentration-dependent inhibitory effect on migration and motility of CL1-0 cells in the absence of cytotoxicity. The results of a gelatin zymography assay showed that A. cinnamomea suppressed the activity of matrix metalloproteinase (MMP)-2 and MMP-9 in a concentration-dependent manner. Western blot results demonstrated that treatment with A. cinnamomea decreased the expression of MMP-9 and MMP-2; while the expression of the endogenous inhibitors of these proteins, i.e., tissue inhibitors of MMP (TIMP-1 and TIMP-2) increased. Two major compounds from EEAC codycepin and zhankuic acid A alone and together inhibited MMP-9 and MMP-2 expressions. Further investigation revealed that A. cinnamomea suppressed the phosphorylation of p38, and JNK1/2. A. cinnamomea also suppressed the expressions of PI3K and phosphorylation of AKT. This is the first report confirming the anti-migration activity of this potentially beneficial mushroom against human lung adenocarcinoma CL1-0.",
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