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心脏毒素III通过丝裂原活化蛋白激酶（MAPK）和基质金属蛋白酶（MMP）信号通路抑制口腔癌细胞的增殖和迁移。

Cardiotoxin III inhibits proliferation and migration of oral cancer cells through MAPK and MMP signaling.

作者信息

Yen Ching-Yu, Liang Shih-Shin, Han Lo-Yi, Chou Han-Lin, Chou Chon-Kit, Lin Shinne-Ren, Chiu Chien-Chih

机构信息

Department of Oral and Maxillofacial Surgery, Chi-Mei Medical Center, Tainan 710, Taiwan.

出版信息

ScientificWorldJournal. 2013 Apr 8;2013:650946. doi: 10.1155/2013/650946. Print 2013.

DOI:10.1155/2013/650946
PMID:23710144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3654281/
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.

摘要

从台湾眼镜蛇（Naja naja atra）蛇毒中分离出的心脏毒素III（CTXIII），此前已被发现可诱导多种癌症细胞凋亡。早期转移是口腔癌进展的典型特征。调节口腔癌细胞的迁移行为是口腔癌治疗方法之一。在本研究中，探讨了CTXIII对口腔癌迁移可能的调节作用。以口腔鳞状癌细胞Ca9-22为例，CTXIII处理以剂量依赖方式降低细胞活力。在伤口愈合试验中，CTXIII以剂量和时间依赖方式减弱Ca9-22细胞的迁移。CTXIII处理后，MMP-2和MMP-9蛋白表达下调，JNK和p38-MAPK的磷酸化增加，而与ERK磷酸化无关。总之，CTXIII对口腔癌细胞具有抗增殖和抗迁移作用，涉及p38-MAPK和MMP-2/-9途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/40ddae7040c8/TSWJ2013-650946.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/4ac33915278f/TSWJ2013-650946.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/eca4cf0e84d9/TSWJ2013-650946.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/4d5d8b193216/TSWJ2013-650946.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/1558852781cc/TSWJ2013-650946.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/40ddae7040c8/TSWJ2013-650946.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/4ac33915278f/TSWJ2013-650946.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/eca4cf0e84d9/TSWJ2013-650946.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/4d5d8b193216/TSWJ2013-650946.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/1558852781cc/TSWJ2013-650946.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8bc/3654281/40ddae7040c8/TSWJ2013-650946.005.jpg

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