Different affinity of nuclear factor-kappa B proteins to DNA modified by antitumor cisplatin and its clinically ineffective trans isomer
Version of Record online: 23 JAN 2014
© 2014 FEBS
The FEBS Journal
Volume 281, Issue 5, pages 1393–1408, March 2014
How to Cite
Kasparkova, J., Thibault, T., Kostrhunova, H., Stepankova, J., Vojtiskova, M., Muchova, T., Midoux, P., Malinge, J.-M. and Brabec, V. (2014), Different affinity of nuclear factor-kappa B proteins to DNA modified by antitumor cisplatin and its clinically ineffective trans isomer. The FEBS Journal, 281: 1393–1408. doi: 10.1111/febs.12711
- Issue online: 3 MAR 2014
- Version of Record online: 23 JAN 2014
- Accepted manuscript online: 13 JAN 2014 08:24AM EST
- Manuscript Accepted: 13 DEC 2013
- Manuscript Revised: 6 NOV 2013
- Manuscript Received: 25 AUG 2013
- Czech Science Foundation. Grant Number: 301/10/0598
- Ligue Nationale Française contre le Cancer
- Ministère de l'Enseignement supérieur et de la Recherche
- Palacky University in Olomouc. Grant Number: PrF 2013 017
- Centre of the Region Hana for Biotechnological and Agricultural Research. Grant Number: ED0007/01/01
Fig. S1. Binding of NF-κB to purified κB ODN containing one platinum adduct in the absence of unplatinated duplexes.
Fig. S2. Binding of NF-κB to purified κB ODN containing one platinum adduct in the absence of unplatinated duplexes, as well as binding of NF-κB to globally platinated DNA containing the κB site (competition experiments).
Fig. S3. Binding of native complex of NF-кB from whole cell extracts to the 22-bp oligonucleotide duplexes. Whole cell extracts were prepared from nonstimulated HeLa cells or stimulated with the cytokine IL-1α.
Fig. S4. Binding of NF-κB to globally platinated DNA lacking the κB site.
Fig. S5. In vitro complexation between Lipofectamine 2000 and the decoy ODN.
Fig. S6. The effect of platination on the decoy activity of the NF-кB dumbbell ODN.
Fig. S7. Western blot analyses of levels of Bcl-2, Bcl-XL and c-IAP1 proteins in A2780 cells.
Fig. S8. Effects of cisplatin and NF-κB inhibitor JSH-23 on activation of the apoptotic pathway and necrosis (black bars) in A2780 cells determined by DNA fragmentation ELISA.
Fig. S9. Effects of cisplatin and JSH-23 on cell cycle distribution.
Table S1A. Relative levels of expression of NF-κB target antiapoptotic proteins after treatment of A2780 cells with various doses of cisplatin.
Table S1B. Relative levels of expression of antiapoptotic protein Bcl-XL after treatment of A2780 cells with cisplatin, JSH-23 and a combination of both.
Table S2. Cytotoxicity [IC50 mean values (μm)] obtained for cisplatin, transplatin and NF-κB inhibitor JSH-23 in A2780 cells.
Table S3. CI values obtained by analysis of combinational effect of cisplatin and NF-κB inhibitor JSH-23 in A2780 cells.
Table S4. CI values obtained by analysis of combinational effect of transplatin and NF-κB inhibitor JSH-23 in A2780 cells.
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