EGCG sensitizes human nasopharyngeal carcinoma cells to TRAIL-mediated apoptosis by activation NF-κB

Neoplasma. 2017;64(1):74-80. doi: 10.4149/neo_2017_109.

Abstract

Aim of presented study was to investigate whether EGCG could sensitize TRAIL resistant NPC cells to TRAIL-mediated apoptosis. Three human NPC cell-lines CNE-1, CNE-2, C666-1 and a non-transformed nasopharyngeal epithelium cell-line NP-69 were treated with EGCG or/and TRAIL. The apoptosis and TRAIL receptors were determined by flow cytometric analysis. The protein expression was determined by western blotting. Mitochondrial transmembrane potential was dertemined by DiOC6 (3). C666-1 cell-line was the only one that resistant to TRAIL and selected to be treated with EGCG. ECGC could sensitize C666-1 to TRAIL. Combinatorial treatments led to decrease expression of Bcl-XL, Bcl-2, FADD and FLIP and enhance activation of capase-3, -8, -9. The DiOC6 (3) negative cell rate was increased and p65 of NF-κB, XIAP and survivin expression was reduced by the combination treatment.In summary, EGCG sensitizes NPC cells to TRAIL-mediated apoptosis via modulation of extrinsic and intrinsic apoptotic pathways and inhibition of NF-κB activation.

Keywords: EGCG; TRAIL; apoptosis NF-κB.; nasopharyngeal carcinoma.

MeSH terms

  • Apoptosis*
  • Catechin / analogs & derivatives*
  • Catechin / pharmacology
  • Cell Line, Tumor
  • Humans
  • NF-kappa B / metabolism*
  • Nasopharyngeal Carcinoma / metabolism*
  • TNF-Related Apoptosis-Inducing Ligand / metabolism*

Substances

  • NF-kappa B
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human
  • Catechin
  • epigallocatechin gallate