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Title: Control of hypoxia-induced tumor cell adhesion by cytophilic human catalase.
Authors: Yata, Tomoya
Nishikawa, Makiya  kyouindb  KAKEN_id
Nishizaki, Chika
Oku, Masahide  kyouindb  KAKEN_id  orcid (unconfirmed)
Yurimoto, Hiroya  kyouindb  KAKEN_id  orcid (unconfirmed)
Sakai, Yasuyoshi  kyouindb  KAKEN_id
Takakura, Yoshinobu  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 西川, 元也
Keywords: Abnormal cell adhesion
Free radicals
Reactive oxygen species
Recombinant human catalase
Issue Date: 15-Dec-2009
Publisher: Elsevier BV
Journal title: Free radical biology & medicine
Volume: 47
Issue: 12
Start page: 1772
End page: 1778
Abstract: 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.
Rights: c 2009 Elsevier Inc. All rights reserved.
This is not the published version. Please cite only the published version.
DOI(Published Version): 10.1016/j.freeradbiomed.2009.09.027
PubMed ID: 19804819
Appears in Collections:Journal Articles

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