Niacin alleviates TRAIL-mediated colon cancer cell death via autophagy flux activation
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Sung-Wook Kim1, Ju-Hee Lee1, Ji-Hong Moon1, Uddin M.D. Nazim1, You-Jin Lee1, Jae-Won Seol1, Jin Hur1, Seong-Kug Eo1, John-Hwa Lee1, Sang-Youel Park1
1Biosafety Research Institute, Department of Biochemistry, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561–756, South Korea
Sang-Youel Park, e-mail: firstname.lastname@example.org
Keywords: niacin, autophagy, TRAIL, death receptor, mitochondrial membrane potential
Received: June 29, 2015 Accepted: August 26, 2015 Published: October 22, 2015
Niacin, also known as vitamin B3 or nicotinamide is a water-soluble vitamin that is present in black beans and rice among other foods. Niacin is well known as an inhibitor of metastasis in human breast carcinoma cells but the effect of niacin treatment on TRAIL-mediated apoptosis is unknown. Here, we show that niacin plays an important role in the regulation of autophagic flux and protects tumor cells against TRAIL-mediated apoptosis. Our results indicated that niacin activated autophagic flux in human colon cancer cells and the autophagic flux activation protected tumor cells from TRAIL-induced dysfunction of mitochondrial membrane potential and tumor cell death. We also demonstrated that ATG5 siRNA and autophagy inhibitor blocked the niacin-mediated inhibition of TRAIL-induced apoptosis. Taken together, our study is the first report demonstrating that niacin inhibits TRAIL-induced apoptosis through activation of autophagic flux in human colon cancer cells. And our results also suggest that autophagy inhibitors including genetic and pharmacological tools may be a successful therapeutics during anticancer therapy using TRAIL.
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