Abstract
Abstract Damnacanthal is an anthraquinone isolated from the root of Morinda citrifolia L. (Noni) and exhibits many pharmacological properties including anti-cancer activity. It has been reported that Damnacanthal targets several signal transduction proteins related to cell growth inhibition or apoptosis. However, the molecular mechanisms by which Damnacanthal affects anti-cancer activity has not been elucidated in details. Cyclin D1 is the important regulatory protein in cell cycle progression and overexpressed in many cancer cells. In this study, we investigated the molecular mechanism of damnacanthal on cyclin D1 expression. We found that damnacanthal inhibited growth of several cancer cells (HCT-116, HT-29, MCF-7 and PC-3) in a dose- and time- dependent manner with decreasing in cyclinD1 protein expression. Damnacanthal did not change mRNA of cyclin D1, rather it suppressed cyclin D1 expression at the post-translational level. Subsequent experiments with dominant negative mutant cyclin D1 suggest that cyclin D1 at the lysine sites plays a pivotal role in damnacanthal-mediated cyclin D1 suppression. Furthermore, damnacanthal was encapsulated in self-assembled chitosan nanoparticle to improve both physicochemical and biological activities. Our results suggest that encapsulated damnacanthal exhibits better activity in cell growth inhibition, compared to non-encapsulated damnacanthal. Damnacanthal nanoformulation has potential to be a candidate for development of chemoprevention or therapeutic agent for cancers. Grant support: This work was supported by grant from the University of Tennessee Center of Excellence in Livestock Diseases and Human Health and The Thailand Research Fund (TRF) and Faculty of Pharmacy, Mahidol University (IRG5780007). Citation Format: Pakin Sukamporn, Pleumchitt Rojanapanthu, Seung Joon Baek. Damnacanthal and its nanoformulation suppress cyclin D1 expression. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2625A.
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