δ-Tocotrienol induces apoptosis and inhibits proliferation of nasopharyngeal carcinoma cells

Food Funct. 2021 Jul 21;12(14):6374-6388. doi: 10.1039/d1fo00461a. Epub 2021 May 31.

Abstract

Nasopharyngeal carcinoma has a notably high incidence rate in Southern China, Southeast Asia, North Africa, Middle East, and the Arctic. δ-Tocotrienol is abundant in cereal and has some health benefits. In our recent study, we showed that δ-tocotrienol exerted anti-inflammatory effects in murine macrophages in vitro. The aim of this study was to further investigate the chemopreventive effects of δ-tocotrienol on human CNE1 cells. We showed that δ-tocotrienol induced apoptosis and cell cycle arrest at G0/G1 and M phases in nasopharyngeal carcinoma cells. Microarray analysis revealed that after CNE1 cells were treated with δ-tocotrienol, 169 genes were up-regulated and 167 down-regulated. ERK1/2 was shown to play a vital role in cell cycle arrest by gene chips. The results suggest that δ-tocotrienol induces cell cycle arrest in CNE1 cells via the p16/CDK4/cyclin D1 signaling pathway. Western blots showed that CNE1 apoptosis was related to dysregulated expression of Bax-2 and Bcl-2. Furthermore, caspase-3, -8, -9 up-regulation was related to the apoptotic effect of δ-tocotrienol; therefore, δ-tocotrienol triggers apoptosis in CNE1 cells through caspase-3 signaling. δ-Tocotrienol may potentially be developed as an anti-cancer agent in the management of nasopharyngeal carcinoma.

MeSH terms

  • Animals
  • Anticarcinogenic Agents / pharmacology
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • China
  • Cyclin D1 / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MAP Kinase Signaling System / drug effects
  • Mice
  • Nasopharyngeal Carcinoma / drug therapy*
  • Nasopharyngeal Carcinoma / genetics
  • Nasopharyngeal Carcinoma / metabolism
  • Nasopharyngeal Neoplasms / drug therapy*
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction / drug effects
  • Vitamin E / analogs & derivatives*
  • Vitamin E / pharmacology

Substances

  • Anticarcinogenic Agents
  • Proto-Oncogene Proteins c-bcl-2
  • Cyclin D1
  • Vitamin E
  • tocotrienol, delta
  • Caspase 3