Synergy between enzastaurin doxorubicin in inducing melanoma apoptosis
Article first published online: 7 AUG 2013
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Pigment Cell & Melanoma Research
Volume 26, Issue 6, pages 900–911, November 2013
How to Cite
Romano, S., Nappo, G., Calì, G., Wang, S. Y.-S., Staibano, S., D'Angelillo, A., Ilardi, G., Sorrentino, A., Di Pace, A. L., Siano, M., Bisogni, R. and Romano, M. F. (2013), Synergy between enzastaurin doxorubicin in inducing melanoma apoptosis. Pigment Cell & Melanoma Research, 26: 900–911. doi: 10.1111/pcmr.12144
- Issue published online: 24 OCT 2013
- Article first published online: 7 AUG 2013
- Accepted manuscript online: 19 JUL 2013 05:22AM EST
- Manuscript Accepted: 16 JUL 2013
- Manuscript Received: 4 FEB 2013
- Italian Association for Cancer Research. Grant Number: 10452
- Cardiovascular Service SRL
Figure S1. Enzastaurin reduced expression levels of phospho-PKC substrates and increases doxorubicin-induced apoptosis in SAN melanoma.
Figure S2. (A) Enzastaurin decreases melanoma growth in a dose–response manner. After a 72 h culture, cell growth was measured by MTS assay (CellTiter 96 AQueous One Solution Cell Proliferation Assay; Promega, WI, USA), according to the manufacturer's protocol. Metabolically active SAN cells were measured by adding 20 μl of MTS tetrazolium to each well. After 2 h of incubation, the plates were analysed using 490 nm absorbance, with a Multilabel Counter (BioTek, Milan, Italy). (B) Dose–response to doxorubicin. Values represent means and standard deviations of 12 experiments (3 for each cell lines, in triplicated) performed with G361, SK-MEL3, A375 and SAN. Cell death was measured after a 48 h incubation with flow cytometry and propidium iodide incorporation.
Figure S3. An electrophoretic mobility shift assay (EMSA) using nuclear extracts prepared from Jurkat cells stimulated with 20 ng/ml TNFα for 1 h, in the absence or the presence of 100 ng/ml H398 antibody.
Figure S4. PKCζ overexpression counteracts enzastaurin-induced increase in doxorubicin-induced cell death.
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