Nisin, an apoptogenic bacteriocin and food preservative, attenuates HNSCC tumorigenesis via CHAC1
Article first published online: 2 OCT 2012
© 2012 The Authors. Cancer Medicine published by Blackwell Publishing Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 1, Issue 3, pages 295–305, December 2012
How to Cite
Cancer Medicine 2012; 1(3): 295-305
- Issue published online: 3 DEC 2012
- Article first published online: 2 OCT 2012
- Manuscript Accepted: 22 AUG 2012
- Manuscript Revised: 21 AUG 2012
- Manuscript Received: 8 JUL 2012
- National Institutes of Health (NIH). Grant Numbers: 3P50 CA097248-07S1, 2R56DE014429
|cam435-sup-0001-FigureS1.pptx||application/mspowerpoint||11610K||Figure S1. Nisin treatment does not alter liver and kidney histological morphology and preloading with nisin reduces tumor volume. (A) Representative hematoxylin and eosin staining of liver and kidney tissue sections from mice administered 150 mg/kg per day of nisin for 3 weeks (n = 3 mice). (B) Tumor volumes for mice administered water (CTRL) or nisin (200 mg/kg per day) for 3 weeks pre- and postinjection of UM-SCC-17B cells. P values for each data set are indicated individually.|
|cam435-sup-0002-FigureS2.pptx||application/mspowerpoint||11610K||Figure S2. Nisin inhibits Cdc2 phosphorylation but promotes PARP and caspase-3 cleavage. Immunoblots showing (A) Cdc2 and p-Cdc2 and (B) active/cleaved PARP and caspase-3 expression in control (CTRL) and nisin-treated UM-SCC-17B cells. β-Actin served as a loading control.|
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