Toxicity of Dimethylmonothioarsinic Acid toward Human Epidermoid Carcinoma A431 Cells

2007 ◽  
Vol 20 (8) ◽  
pp. 1120-1125 ◽  
Author(s):  
Hua Naranmandura ◽  
Kenji Ibata ◽  
Kazuo T. Suzuki
Acta Naturae ◽  
2012 ◽  
Vol 4 (3) ◽  
pp. 88-94 ◽  
Author(s):  
M. A. Savitskaya ◽  
M. S. Vildanova ◽  
O. P. Kisurina-Evgenieva ◽  
E. A. Smirnova ◽  
G. E. Onischenko

Vitamin E derivatives are known to act as agents exhibiting cytotoxity against tumor cells. The effect of vitamin E succinate on human epidermoid carcinoma cell line A431 was investigated in this study using live imaging, immunocytochemistry, and transmission electron microscopy. -Tocopheryl succinate-induced apoptotic cell death in A431 cells was shown to be both dose- and time-dependent. The hyperproduction of reactive oxygen species, changes in size, shape and ultrastructural characteristics of mitochondria followed by the release of cytochrome c from mitochondria to cytosol were observed. These results suggest that -tocopheryl succinate induces apoptosis that occurs via the mitochondrial pathway. Mitochondria are shown to be crucial targets in -tocopheryl succinate-induced caspase-dependent cell death in human carcinoma A431 cells.


2017 ◽  
Vol 12 (3) ◽  
pp. 299
Author(s):  
Lei Zheng ◽  
Hao He ◽  
Xuji Shen ◽  
Yanping Sun

<p class="Abstract">The aim of this study was to examine the anti-proliferation and anti-migration effect of Centipede Scolopendra extracts (CSE) on human epidermoid carcinoma cells (high-EGFR expression) A431 and elucidate the underlying signaling mechanisms. MTT and colony formation assays were used. Migration and invasion potential of A431 cells were examined by wound-healing assays and matrigel invasion chamber assays. To investigate the underlying molecular mechanisms, we used ELISA to analyze the expression of EGF, Western blotting to analyze the expression of MMP2 (matrix metalloproteinase 2), MMP9 and EGFR, PCR to analyze the mRNA expression of EGFR pretreated with CSE. The results showed that CSE effectively inhibited the proliferation of A431. Furthermore, CSE-mediated cell cycle arrest in S phase. We also observed that CSE treatment led to down-regulation of MMP2 and MMP9 and suppress the migration and invasion in A431. CSE exerted its anti-proliferation and anti-migration by targeting EGFR and related metastasis factors, thus could be a useful therapeutic candidate for high-EGFR expression cancer intervention.</p><p class="Abstract"><strong>Video Clip of Methodology</strong>:</p><p class="Abstract">Cell migration and invasion assay: 2 min 41 sec   <a href="https://www.youtube.com/v/fg27Xn0talE">Full Screen</a>   <a href="https://www.youtube.com/watch?v=fg27Xn0talE">Alternate</a>   </p>


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