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. 2015 Jan 23;15:19. doi: 10.1186/s12885-014-1003-1

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© Park et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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HNHA induced cytochrome c-dependent, caspase-dependent apoptotic death in RCCs. Subcellular fractionation showed that the Bax level was increased, and cytochrome c release into the cytosol was enhanced by HNHA, in Caki-1 (A) and A 498 cells (B). Immunofluorescent cytochemical staining showed that cytochrome c was translocated and accumulated in the nucleus, suggesting that HNHA induced apoptosis through a cytochrome-c-dependent pathway. (C, D) Western blot analysis after subcellular fractionation confirmed that cytochrome c was translocated into the nucleus after HNHA treatment (E, F).