Table of Contents Author Guidelines Submit a Manuscript
The Scientific World Journal
Volume 2013, Article ID 650946, 5 pages
http://dx.doi.org/10.1155/2013/650946
Research Article

Cardiotoxin III Inhibits Proliferation and Migration of Oral Cancer Cells through MAPK and MMP Signaling

1Department of Oral and Maxillofacial Surgery, Chi-Mei Medical Center, Tainan 710, Taiwan
2School of Dentistry, Taipei Medical University, Taipei 110, Taiwan
3Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan
4Department of Biotechnology, Kaohsiung Medical University, Kaohsiung 807, Taiwan
5Department of Medicinal and Applied Chemistry, Kaohsiung Medical University, Kaohsiung 807, Taiwan

Received 18 February 2013; Accepted 12 March 2013

Academic Editors: H.-W. Chang, L.-Y. Chuang, S. Guleria, and S. Yasmin

Copyright © 2013 Ching-Yu Yen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cardiotoxin III (CTXIII), isolated from the snake venom of Formosan cobra Naja naja atra, has previously been found to induce apoptosis in many types of cancer. Early metastasis is typical for the progression of oral cancer. To modulate the cell migration behavior of oral cancer is one of the oral cancer therapies. In this study, the possible modulating effect of CTXIII on oral cancer migration is addressed. In the example of oral squamous carcinoma Ca9-22 cells, the cell viability was decreased by CTXIII treatment in a dose-responsive manner. In wound-healing assay, the cell migration of Ca9-22 cells was attenuated by CTXIII in a dose- and time-responsive manner. After CTXIII treatment, the MMP-2 and MMP-9 protein expressions were downregulated, and the phosphorylation of JNK and p38-MAPK was increased independent of ERK phosphorylation. In conclusion, CTXIII has antiproliferative and -migrating effects on oral cancer cells involving the p38-MAPK and MMP-2/-9 pathways.