Abstract

Pycnidione, a small tropolone first isolated from the fermented broth of Theissenia rogersii 92031201, exhibits antitumor activities through an undefined mechanism. The present study evaluated the effects and mechanisms of pycnidione on the growth and death of A549 human lung cancer cells. Pycnidione significantly inhibited the proliferation of A549 cells in a concentration-dependent manner, with a 50% growth inhibition (GI 50) value of approximately 9.3 nM at 48 h. Pycnidione significantly decreased the expression of cyclins D1 and E and induced G 1-phase cell cycle arrest and a subsequent increase in the sub-G 1 phase population. Pycnidione also markedly reduced the expression of survivin and activated caspase-8 and -3, increased reactive oxygen species (ROS) generation, caused the collapse of the mitochondrial membrane potential (MMP), and enhanced PAI-1 production, thus triggering apoptosis in the A549 cells. Taken together, pycnidione exerts anti-proliferative effects on human lung cancer cells through the induction of cell cycle arrest and apoptosis. Therefore, testing of its effects in vivo is warranted to evaluate its potential as a therapeutic agent against lung cancer.

Original languageEnglish
Pages (from-to)23-30
Number of pages8
JournalChemico-Biological Interactions
Volume197
Issue number1
DOIs
Publication statusPublished - Apr 15 2012

Fingerprint

Cell Cycle Checkpoints
Fungi
Lung Neoplasms
Cells
Apoptosis
Tropolone
Cyclin E
Caspase 8
Mitochondrial Membrane Potential
Cyclin D1
Plasminogen Activator Inhibitor 1
Growth
Caspase 3
pycnidione
Reactive Oxygen Species
Membranes
Testing
Population

Keywords

  • Apoptosis
  • Cell cycle arrest
  • Fungus
  • Lung cancer
  • Pycnidione
  • Theissenia rogersii

ASJC Scopus subject areas

  • Toxicology

Cite this

Pycnidione, a fungus-derived agent, induces cell cycle arrest and apoptosis in A549 human lung cancer cells. / Hsiao, Che Jen; Hsiao, Shih Hsin; Chen, Wei Lin; Guh, Jih Hwa; Hsiao, George; Chan, Yen Ju; Li, Zong-Huei; Chung, Chi Li.

In: Chemico-Biological Interactions, Vol. 197, No. 1, 15.04.2012, p. 23-30.

Research output: Contribution to journalArticle

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