Wogonoside induces apoptosis in human non-small cell lung cancer A549 cells by promoting mitochondria dysfunction

Biomed Pharmacother. 2018 Oct:106:593-598. doi: 10.1016/j.biopha.2018.06.077. Epub 2018 Jul 11.

Abstract

Non-small cell lung cancer (NSCLC) is one of the most prevailing malignancies worldwide. It has been previously shown that wogonoside exerts anti-tumor activities in various kinds of human cancers. But its role in NSCLC remains elusive. In the present study, we determined the anti-tumor effect of wogonoside in human NSCLC A549 cells. We found that wogonoside effectively inhibits A549 cell viability through inducing cell cycle arrest and apoptosis. Moreover, administration of wogonoside by intraperitoneal injection inhibits the growth of A549 cell xenografts in athymic nude mice. Additionally, mitochondrial membrane potential was disrupted and cytochrome c was released to cytosol in the wogonoside-treated A549 cells. Finally, we found that AMPK/mTOR signaling might be implicated in the anti-NSCLC efficacy of wogonoside. Therefore, we may assume that wogonoside may be considered as a potential therapeutic agent for the treatment of NSCLC.

Keywords: AMPK/mTOR signaling; Apoptosis; Mitochondria; Non-small cell lung cancer; Viability; Wogonoside.

MeSH terms

  • A549 Cells
  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Cell Cycle Checkpoints / drug effects
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cytochromes c / metabolism
  • Dose-Response Relationship, Drug
  • Flavanones / pharmacology*
  • Glucosides / pharmacology*
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Male
  • Membrane Potential, Mitochondrial / drug effects
  • Mice, Inbred BALB C
  • Mice, Nude
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism
  • Time Factors
  • Tumor Burden / drug effects
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents, Phytogenic
  • Flavanones
  • Glucosides
  • Cytochromes c
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • wogonoside