Record Details
Field | Value |
---|---|
Title | An epigenetic perspective on pharmacologic ascorbate in colon cancer |
Names |
Kaiser, Matthew Carl
(creator) Rajendran, Praveen (creator) Dashwood, Mohaiza W. (creator) Levine, Mark A. (creator) Michels, Alexander (creator) Frei, Balz (creator) Dashwood, Roderick H. (creator) |
Date Issued | 2013-04-18 (iso8601) |
Note | Honors Bachelor of Science (HBS) |
Abstract | Aim: There is growing interest in pharmacologic ascorbate (Asc) and its therapeutic properties (Levine et al. Adv Nutr 2011;2:78). W e examined cell viability, histone deacetylase (HDAC) expression, and related protein modifications in cancer versus non- cancer colon epithelial cells following exposure to Asc. Methods: MTT assays were conducted in HCT116 colon cancer and CCD841 non-transformed colonic epithelial cells treated with 0.25 to 16 mM Asc or ascorbate-2-phosphate (AAp), in the presence and absence of catalase (CAT, 280 U/mg), or with 5 to 160 μM H₂O₂. Cell lysates obtained 6 h and 24 h post-treatment were immunoblotted as reported by Rajendran et al. Mol Cancer 2011;10:68. Results: In MTT assays, IC₅₀ data were as follows: 8 mM Asc (CCD841); 3 mM Asc (HCT116), >50mM AAp (HCT116), and 65 μM H₂O₂ (HCT116). CAT protected against both Asc- and H₂O₂- induced cytotoxicity. At 6 h, Asc and H₂O₂ altered the expression of HDACs (HDAC4, HDAC6, SIRT3) and enhanced the acetylation of histone (H3, H4) and non-histone proteins (tubulin, p53). Conclusions: Asc was more cytotoxic to colon cancer cells than non-cancer cells. Findings with the non-H₂O₂ producing compound AAp, and with CAT, implicated H₂O₂ in Asc-induced cytotoxicity. Asc was shown, for the first time, to alter epigenetic end-points related to HDAC changes in colon cancer cells. |
Genre | Video |
Topic | Kaiser |
Identifier | http://hdl.handle.net/1957/55927 |