Cinnamaldehyde induces apoptosis and reverses epithelial-mesenchymal transition through inhibition of Wnt/β-catenin pathway in non-small cell lung cancer

Int J Biochem Cell Biol. 2017 Mar:84:58-74. doi: 10.1016/j.biocel.2017.01.005. Epub 2017 Jan 16.

Abstract

Cinnamaldehyde, the main chemical component of the essential oil separated from the traditional herb Cinnamomum cassia, has been demonstrated to be an efficient cytotoxic agent against several human cancers. The present experiment showed that cinnamaldehyde dose-dependently depresses the proliferation of three types of NSCLC cells and induces cell apoptosis in vitro and in vivo. Moreover, cinnamaldehyde attenuated CoCl2-induced EMT and decreased matrix metalloprotease (MMP) family while the in vivo study showed the same trend. Mechanistically, cinnamaldehyde imitated the suppressive effect of XAV939 on cell motility and EMT which could be impaired by LiCl. Collectively, our research demonstrated for the first time that cinnamaldehyde is able to inhibit NSCLC cell growth by inducing apoptosis and reverse EMT through terminating Wnt/β-catenin pathway, which might supply further insight into cinnamaldehyde-mediated anti-tumor effect against NSCLC for better prognosis.

Keywords: Apoptosis; Cinnamaldehyde; EMT; NSCLC; Wnt/β-catenin pathway.

MeSH terms

  • A549 Cells
  • Acrolein / administration & dosage
  • Acrolein / analogs & derivatives*
  • Acrolein / pharmacology
  • Animals
  • Antineoplastic Agents, Phytogenic / administration & dosage
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Cobalt / toxicity
  • Dose-Response Relationship, Drug
  • Epithelial-Mesenchymal Transition / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasm Invasiveness
  • Wnt Signaling Pathway / drug effects
  • Xenograft Model Antitumor Assays
  • beta Catenin / metabolism

Substances

  • Antineoplastic Agents, Phytogenic
  • CTNNB1 protein, human
  • beta Catenin
  • Cobalt
  • Acrolein
  • cobaltous chloride
  • cinnamaldehyde