Differential susceptibilities of human lung, breast and skin cancer cell lines to killing by five sea anemone venoms

Ramezanpour M (1), Burke da Silva K (2), Sanderson BJS (3)

(1) Department of Medical Biotechnology, School of Medicine, Flinders University of South Australia, Adelaide, Australia; (2) School of Biological Sciences, Flinders University of South Australia, Adelaide, Australia; (3) Department of Medical Biotechnology, School of Medicine, Flinders University of South Australia, Adelaide, Australia.

Abstract: Although sea anemones are well known for being rich sources of toxins, including cytolysins and neurotoxins, their venoms and toxins have been poorly studied. In the present study, the venoms from five sea anemones (Heteractis crispa, Heteractis magnifica, Heteractis malu, Cryptodendrum adhaesivum andEntacmaea quadricolor) were obtained by the milking technique, and the potential of these venoms to kill cancer cells was tested on three cell lines (A549 lung cancer, T47D breast cancer and A431 skin cancer). The total protein level in the crude extract was determined by the bicinchoninic acid (BCA) protein assay. The cytotoxicity on different cell lines was assayed using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay which measures survival based on the detection of mitochondrial activity and by the crystal violet assay, which measures survival based on the ability of cells to remain adherent to microplates. The results indicate that the sea anemone venom is cytotoxic to human cancer cells. The A549 cell line was the most sensitive of the cell lines tested with a significant reduction in viability observed at 40 μg/mL. H. malu, C. adhaesivum andE. quadricolor had a significant inhibitory effect on A431 cells. Furthermore, H. malu andC. adhaesivum had a significant inhibitory effect on T47D cell line at 40 μg/mL. In conclusion, the sea anemone venoms tested have the potential to be developed as anticancer agents.

Key words: sea anemone venoms, cytolysin, cancer cell line.

COPYRIGHT

© CEVAP 2012

SUBMISSION STATUS

Received: July 14, 2011.

Accepted: November 21, 2011.

Abstract published online: November 28, 2011.

Full paper published online: May 31, 2012.

CONFLICTS OF INTEREST

The authors declare no conflicts of interest.

FINANCIAL SOURCE

A Faculty of Health Sciences Underwriting Grant provide partial financial support for this work.

CORRESPONDENCE TO

Barbara J. S. Sanderson, Department of Medical Biotechnology, School of Medicine, Flinders University of South Australia, Bedford Park, SA 5042, Australia. Phone: +61872218556. Fax: +61872218555. Email: barbara.sanderson@flinders.edu.au.