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EGCG sensitizes human nasopharyngeal carcinoma cells to TRAIL-mediated apoptosis by activation NF-κB
Author(s) -
Ping Li,
Shu Li,
Tyler Yin,
Jun Li,
Lu Wang,
Chun-Ming Huang,
Xiaolong Yang
Publication year - 2016
Publication title -
neoplasma
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.628
H-Index - 50
eISSN - 1338-4317
pISSN - 0028-2685
DOI - 10.4149/neo_2017_109
Subject(s) - nasopharyngeal carcinoma , xiap , apoptosis , survivin , fadd , tradd , traf2 , cell culture , cancer research , microbiology and biotechnology , chemistry , signal transduction , jurkat cells , biology , death domain , programmed cell death , caspase , immunology , t cell , medicine , immune system , biochemistry , tumor necrosis factor receptor , genetics , radiation therapy
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.

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