TY - JOUR
T1 - Ursodeoxycholic acid can suppress deoxycholic acid-induced apoptosis by stimulating Akt/PKB-dependent survival signaling
AU - Im, Eunok
AU - Akare, Sandeep
AU - Powell, Ashley
AU - Martinez, Jesse D.
N1 - Funding Information:
This work was supported by the National Institutes of Health grant CA72008. A. A. Powell was supported in part by National Institutes of Health training grant T32CA09213. We acknowledge Dr Chiu-Hsieh Hsu, PhD, for help in statistical analysis. E. Im is currently affiliated with Schepens Eye Research Institute, Harvard Medical School, Boston, MA 02114. A. Powell is currently affiliated with the Department of Radiation Oncology, CCSR-South, Stanford, CA 94305. Address correspondence to J. D. Martinez, University of Arizona, Arizona Cancer Center, 1515 N. Campbell Ave., Tucson, Arizona 85724. E-mail: jmartinez@azcc.arizona.edu.
PY - 2005
Y1 - 2005
N2 - The nontoxic bile acid ursodeoxycholic acid (UDCA) is reported to be an anti-apoptotic agent with efficacy against a variety of death stimuli including the cytotoxic bile acid deoxycholic acid (DCA). To gain insight into this anti-apoptotic property, we tested UDCA for its ability to protect the colon carcinoma-derived cell line HCT116 against DCA-induced apoptosis. We found that UDCA could suppress DCA-induced apoptosis in a time- and dose-dependent manner and that this effect correlated with Akt phosphorylation. Importantly, UDCA lost its ability to protect cells from DCA-induced cell death when Akt activity was suppressed genetically using a dominant negative Akt mutant or when PI3K activity was inhibited pharmacologically. These results suggest that UDCA can protect HCT116 cells against DCA-induced apoptosis by stimulating Akt-dependent survival signaling.
AB - The nontoxic bile acid ursodeoxycholic acid (UDCA) is reported to be an anti-apoptotic agent with efficacy against a variety of death stimuli including the cytotoxic bile acid deoxycholic acid (DCA). To gain insight into this anti-apoptotic property, we tested UDCA for its ability to protect the colon carcinoma-derived cell line HCT116 against DCA-induced apoptosis. We found that UDCA could suppress DCA-induced apoptosis in a time- and dose-dependent manner and that this effect correlated with Akt phosphorylation. Importantly, UDCA lost its ability to protect cells from DCA-induced cell death when Akt activity was suppressed genetically using a dominant negative Akt mutant or when PI3K activity was inhibited pharmacologically. These results suggest that UDCA can protect HCT116 cells against DCA-induced apoptosis by stimulating Akt-dependent survival signaling.
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U2 - 10.1207/s15327914nc5101_15
DO - 10.1207/s15327914nc5101_15
M3 - Article
C2 - 15749637
AN - SCOPUS:14944350350
VL - 51
SP - 110
EP - 116
JO - Nutrition and Cancer
JF - Nutrition and Cancer
SN - 0163-5581
IS - 1
ER -