Involvement of ROS in Curcumin-induced Autophagic Cell Death

• DOI: 10.4196/kjpp.2011.15.1.1
• Publication Date: 2011-03-19T11:01:17Z
• Authors: Youn Ju Lee; Nam-Yi Kim; Young-Ah Suh; ChuHee Lee
• Keywords: Autophagosome; Bafilomycin; Viability assay

Many anticancer agents as well ionizing radiation have been shown to induce autophagy which is originally described a protein recycling process and recently reported play crucial role in various disorders. In HCT116 human colon cancer cells, we found that curcumin, polyphenolic phytochemical extracted from the plant Curcuma longa, markedly induced conversion of microtubule-associated 1 light chain 3 (LC3)-I LC3-II degradation sequestome-1 (SQSTM1) marker autophagosome degradation. Moreover, curcumin caused GFP-LC3 formation puncta, autophagosome, decrease SQSTM1 level expressing cells. It was further confirmed treatment cells with hydrogen peroxide increase LC3 levels, but these changes by were almost completely blocked presence antioxidant, N-acetylcystein (NAC), indicating leads reactive oxygen species (ROS) production, results development autolysosomal parallel NAC, also diminished bafilomycin A, potent inhibitor autophagosome-lysosome fusion, cell viability assay cucurmin-induced death partially A NAC. We observed NAC abolished curcumin-induced activation extracelluar signal-regulated kinases (ERK) 1/2 p38 mitogen-activated (MAPK), not Jun N-terminal kinase (JNK). However, ERK1/2 MAPK seemed no effect on autophagy, since both changed Taken together, our data suggest ROS resulted autophagic concomitant cell. ROS-dependent MAPK, JNK, might be involved autophagy.