| Autor: |
Yoshida, Chisato, Hishiyama, Kazsuyoshi, Miyazaki, Khosuke, Watanabe, Manami, Kanbe, Masahiro, Yamada, Yuta, Matsuzaki, Keiithi, Miyashita, Kiichi, Kitanaka, Susumu, Miyata, Shohei |
| Zdroj: |
Cancer Science; Feb2010, Vol. 101 Issue 2, p374-378, 5p, 1 Diagram, 7 Graphs |
| Abstrakt: |
We previously reported that many ingenol compounds derived from Euphorbia kansui exhibit topoisomerase inhibitory activity and/or inhibitory activity of cell proliferation. The inhibitory effects of 20- O-(2′ E,4′ Z-decadienoyl) ingenol and 3- O-(2′ E,4′ Z-decadienoyl)-ingenol among these compounds on topoisomerase II activity and on the cell proliferative activity and arrest phase of the cell cycle were studied using a mouse breast cancer (MMT) cell line. Although 20- O-ingenolEZ exerted inhibitory effects on both topoisomerase II activity and cell proliferative activity, 3- O-ingenolEZ exerted inhibitory activity on neither. The 20- O-ingenolEZ-induced cell arrest of MMT-cell proliferation led to a cell cycle arrest in the G2/M phase. Topoisomerase II inhibition can be divided into the poison and catalytic inhibitor types. A checkpoint mechanism is activated when cells are treated with these topoisomerase II inhibitors. Poison-type inhibition occurs via induction of the DNA damage checkpoint and the catalytic-type inhibition occurs via induction of the DNA-decatenation checkpoint, suggestive of distinct checkpoint reactions. 20- O-ingenolEZ inhibited topoisomerase IIα activity through inhibition of ATPase, and induced DNA-decatenation checkpoint without signaling for phosphorylation of H2AX. ( Cancer Sci 2010; 101: 374–378) [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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