Wogonin has multiple anti-cancer effects by regulating c-Myc/SKP2/Fbw7α and HDAC1/HDAC2 pathways and inducing apoptosis in human lung adenocarcinoma cell line A549

PLoS One. 2013 Nov 12;8(11):e79201. doi: 10.1371/journal.pone.0079201. eCollection 2013.

Abstract

Wogonin is a plant monoflavonoid which has been reported to inhibit cell growth and/or induce apoptosis in various tumors. The present study examined the apoptosis-inducing activity and underlying mechanism of action of wogonin in A549 cells. The results showed that wogonin was a potent inhibitor of the viability of A549 cells. Apoptotic protein changes detected after exposure to wogonin included decreased XIAP and Mcl-1 expression, increased cleaved-PARP expression and increased release of AIF and cytochrome C. Western blot analysis showed that the activity of c-Myc/Skp2 and HDAC1/HDAC2 pathways, which play important roles in tumor progress, was decreased. Quantitative PCR identified increased levels of c-Myc mRNA and decreased levels of its protein. Protein levels of Fbw7α, GSK3β and Thr58-Myc, which are involved in c-Myc ubiquitin-dependent degradation, were also analyzed. After exposure to wogonin, Fbw7α and GSK3β expression decreased and Thr58-Myc expression increased. However, MG132 was unable to prevent c-Myc degradation. The present results suggest that wogonin has multiple anti-cancer effects associated with degradation of c-Myc, SKP2, HDAC1 and HDAC2. Its ability to induce apoptosis independently of Fbw7α suggests a possible use in drug-resistance cancer related to Fbw7 deficiency. Further studies are needed to determine which pathways are related to c-Myc and Fbw7α reversal and whether Thr58 phosphorylation of c-Myc is dependent on GSK3β.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism*
  • Adenocarcinoma of Lung
  • Apoptosis / drug effects*
  • Cell Cycle / drug effects
  • Cell Cycle Proteins / metabolism*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • F-Box Proteins / metabolism*
  • F-Box-WD Repeat-Containing Protein 7
  • Flavanones / pharmacology*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • Histone Deacetylase 1 / genetics
  • Histone Deacetylase 1 / metabolism*
  • Histone Deacetylase 2 / genetics
  • Histone Deacetylase 2 / metabolism*
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Membrane Potential, Mitochondrial
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • S-Phase Kinase-Associated Proteins / metabolism*
  • Signal Transduction / drug effects*
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Cell Cycle Proteins
  • F-Box Proteins
  • F-Box-WD Repeat-Containing Protein 7
  • FBXW7 protein, human
  • Flavanones
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • S-Phase Kinase-Associated Proteins
  • Ubiquitin-Protein Ligases
  • GSK3B protein, human
  • Glycogen Synthase Kinase 3 beta
  • Glycogen Synthase Kinase 3
  • Histone Deacetylase 1
  • Histone Deacetylase 2
  • wogonin

Grants and funding

The study was supported by grants from the Ministry of Science and Technology of Guizhou Province, China ([2012] 7006 and NY [2011]3072); Guangzhou Medical College (2012C16); the Foundation for Young Scientists of Guangzhou Educational Committee (2012C118). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.