Suppression of cell growth, migration and drug resistance by ethanolic extract of antrodia cinnamomea in human lung cancer A549 cells and C57BL/6J allograft tumor model

Chi Han Wu, Fon Chang Liu, Chun Hsu Pan, Ming Tsung Lai, Shou Jen Lan, Chieh Hsi Wu, Ming Jyh Sheu

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from Antrodia cinnamomea (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5′-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.

Original languageEnglish
Article number791
JournalInternational Journal of Molecular Sciences
Volume19
Issue number3
DOIs
Publication statusPublished - Mar 9 2018

Fingerprint

Antrodia
Cell growth
Drug Resistance
lungs
Cell Movement
Allografts
Tumors
Lung Neoplasms
drugs
tumors
cancer
retarding
proteins
Proteins
Growth
cells
Pharmaceutical Preparations
Cyclin D1
Cells
Neoplasms

Keywords

  • Anti-migration
  • Anti-proliferation
  • Antrodia cinnamomea
  • Lung cancer
  • Paclitaxel resistance

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Suppression of cell growth, migration and drug resistance by ethanolic extract of antrodia cinnamomea in human lung cancer A549 cells and C57BL/6J allograft tumor model. / Wu, Chi Han; Liu, Fon Chang; Pan, Chun Hsu; Lai, Ming Tsung; Lan, Shou Jen; Wu, Chieh Hsi; Sheu, Ming Jyh.

In: International Journal of Molecular Sciences, Vol. 19, No. 3, 791, 09.03.2018.

Research output: Contribution to journalArticle

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abstract = "The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from Antrodia cinnamomea (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5′-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.",
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AU - Wu, Chi Han

AU - Liu, Fon Chang

AU - Pan, Chun Hsu

AU - Lai, Ming Tsung

AU - Lan, Shou Jen

AU - Wu, Chieh Hsi

AU - Sheu, Ming Jyh

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