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The anti-tumor effect of Euchema serra agglutinin on colon cancer cells in vitro and in vivo

Fukuda, Yukia; Sugahara, Takuyaa; Ueno, Masashia; Fukuta, Yusukeb; Ochi, Yukaria; Akiyama, Koichic; Miyazaki, Tatsuhikod; Masuda, Seizoe; Kawakubo, Akihirof; Kato, Keiichib

doi: 10.1097/01.cad.0000224458.13651.b4
PRECLINICAL REPORTS
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Eucheuma serra agglutinin (ESA) is a lectin derived from a marine red alga E. serra and binds specifically to mannose-rich sugar chains. Previous reports have indicated that ESA associates with several cancer cells via sugar chains on cell surfaces and induces apoptotic cell death. In this study, we investigated the effect of ESA on Colon26 mouse colon adenocarcinoma cells both in vitro and in vivo. ESA induced cell death against Colon26 cells in vitro, and the expression of caspase-3 and the translocation of phosphatidylserine in ESA-treated Colon26 cells suggested that this cell death was induced through apoptosis. An intravenous injection of ESA significantly inhibited the growth of Colon26 tumors in BALB/c mice; moreover, DNA fragmentation was detected in tumor cells following ESA treatment. These results indicated that ESA is effective as an anti-cancer drug not only in vitro but also in vivo. The side-effects of ESA were not considered to be serious because the decrease in body weight of the mice injected with it was negligible. These observations suggest that ESA has the potential to be an effective anti-tumor drug.

Faculties of aAgriculture

bEngineering

cIntegrated Center for Sciences Tarumi Station, Ehime University, Matsuyama

dFaculty of Medicine

eIntegrated Center for Sciences Shigenobu Station, Ehime University, Toon

fYamaki Co., Iyo, Ehime, Japan

Correspondence to K. Kato, Faculty of Engineering, Ehime University, 6 Bunkyou-cho, Matsuyama, 790-8577.

Tel/fax: +81 89 927 9928

and Sugahara, Faculty of Engineering, Ehime University, 3-5-7 Tarumi, Matsuyama, Ehime 790-8566, Japan. Tel/fax: +81 89 946 9863;

e-mail: kato@eng.ehime-u.ac.jp and mars95@agr.ehime-u.ac.jp

Received 8 February 2006 Accepted 30 May 2006

© 2006 Lippincott Williams & Wilkins, Inc.