ヒト頭頚部癌細胞株におけるＴｏｌｌ‐ｌｉｋｅ　ｒｅｃｅｐｔｏｒ２，４および９の発現と各リガンドに対する反応性

DOI Web Site
  • 田野 智之
    徳島大学大学院分子口腔医学講座口腔腫瘍制御学分野 歯学部口腔外科学第二講座
  • 岡本 正人
    徳島大学大学院分子口腔医学講座口腔腫瘍制御学分野 歯学部口腔外科学第二講座
  • 佐々井 明子
    徳島大学大学院分子口腔医学講座口腔腫瘍制御学分野 歯学部口腔外科学第二講座
  • 吉田 秀夫
    徳島大学大学院分子口腔医学講座口腔腫瘍制御学分野 歯学部口腔外科学第二講座
  • 佐藤 光信
    徳島大学大学院分子口腔医学講座口腔腫瘍制御学分野 歯学部口腔外科学第二講座

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タイトル別名
  • Expression of Toll-like receptor 2,4 and 9 in human head and neck cancer cell lines and their responsiveness against each ligand
  • ヒト トウケイブガン サイボウカブ ニ オケル Toll like receptor 2 4 オヨビ 9 ノ ハツゲン ト カク リガンド ニ タイスル ハンノウセイ

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It has been reported that Toll-like receptors (TLRs) play a significant role in cancer therapy as receptors of bacteria-derived anti-cancer immunotherapeutic agents such as OK-432, Mycobacterium bovis bacillus Calmette-Guerin-cell wall skeleton (BCG-CWS) and CpG-oligode oxynucleotides (ODN). In the current study, we exam inedthe expression of TLRs on 12 human head and neck cancer cell lines and their responsiveness against each TLR ligand. In the quantitative real-time polymerase chain reaction analysis, 6 TLR2-expressing cell lines, 12 TLR4-expressing cell lines, 5 cell lines expressing MD-2, a co-receptor for TLR4, and 11 TLR9-expressing cell lines were observed. Stimulation with peptidoglycan (PGN), a ligand of TLR2 that is an active component of BCG CWS, lipopolysaccaride (LPS) and OK-PSA, an active component of OK-432, that are ligands of TLR4/MD-2, or CpG-DNA, a ligand of TLR9, resulted in the activation of nuclear factor (NF)-kB in the cell lines expressing each receptor. PGN and OK-PSA induced cell-growth inhibi tionand augmented the 5-fluorouracil-induced cell death, while LPS and CpG-DNA enhanced the proliferation of the cancer cells. OK-PSA increased NF-κB activation more slowly than that by LPS. In addition, phosphoryla tionof p38 mitogen-activated protein kinase by OK-PSA was only slight as compared with that by LPS. OK-PSA also induced apoptosis of the cancer cells. It is strongly suggested that active components of OK-432 and BCG CWSmay augment anti-cancer immunity in the hosts as well as may induce growth inhibition and apoptosis of cancer cells via TLRs.

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