Control of hypoxia-induced tumor cell adhesion by cytophilic human catalase.

• 西川, 元也

• Nishikawa, Makiya

• Nishizaki, Chika

• Oku, Masahide

• Yurimoto, Hiroya

• Sakai, Yasuyoshi

• Takakura, Yoshinobu

抄録

Hypoxia-induced reactive oxygen species (ROS)-mediated expression of a variety of genes in endothelial cells has been suggested to be involved in abnormal cell adhesion. To prevent this by accelerated binding of catalase to endothelial cells, human catalase (hCAT), an enzyme catalyzing the decomposition of hydrogen peroxide, was fused with three repeats of arginine-glycine-aspartic acid peptide or nona arginine peptide at the C-terminal to obtain hCAT-(RGD)3 and hCAT-R9, respectively. Human CAT and its derivatives were expressed in yeast Pichia pastoris and purified. The specific activity and secondary structure of hCAT-(RGD)3 and hCAT-R9 were close to those of hCAT, but these derivatives showed higher binding to the mouse aortic vascular endothelial cell line MAEC than hCAT, indicating that they are cytophilic derivatives. Hypoxic treatment of MAEC increased the intracellular ROS level, the binding of mouse melanoma cells, and the activity of transcription factors, hypoxia inducible factor-1 and nuclear factor-kappaB. hCAT-(RGD)3 or hCAT-R9 efficiently inhibited these changes compared with hCAT. These results indicate that cytophilic hCAT-(RGD)3 and hCAT-R9 are effective in inhibiting hypoxia-induced tumor cell adhesion to endothelial cells.

収録刊行物

• Free radical biology & medicine

  Free radical biology & medicine 47 (12), 1772-1778, 2009-12-15

  Elsevier BV

キーワード

• Abnormal cell adhesion
• Free radicals
• Hypoxia
• Reactive oxygen species
• Recombinant human catalase

詳細情報

• CRID: 1050845760544627584
• NII論文ID: 120001815090
• NII書誌ID: AA11527018
• ISSN: 18734596
• ISSN: 08915849
• HANDLE: 2433/91262
• 本文言語コード: en
• 資料種別: journal article
• データソース種別:
  • IRDB
  • CiNii Articles