Autophagy induction by the 30–100 kDa fraction of areca nut in both normal and malignant cells through reactive oxygen species

doi:10.1016/j.oraloncology.2010.08.002

CNU IR > Pharmacy and Science > Dept. of Biotechnology (including master's program) > Periodical Articles > Item 310902800/25156

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Title:	Autophagy induction by the 30–100 kDa fraction of areca nut in both normal and malignant cells through reactive oxygen species
Authors:	Mei-Huei Lin Wan-Fang Hsieh Wei-Fan Chiang Wen-Zhai Hong Yu-Rung Hsu Yon-Chi Cheng Tai-Chi Chen Kai-Cheng Hsu Pin-Yan Lin Shyun-Yeu Liu Young-Chau Liu
Contributors:	生物科技系
Keywords:	Areca nut ANE 30–100K Autophagy ROS Apoptosis Lymphocyte Fibroblast
Date:	2010-11
Issue Date:	2012-03-30 15:17:46 (UTC+8)
Publisher:	Elsevier
Abstract:	Areca nut (AN) is an addictive carcinogen used by about 200–600 million people worldwide. Some AN components are shown to induce apoptosis; however, we previously demonstrated that AN extract (ANE) and the 30–100 kDa fraction of ANE (ANE 30–100K) induced autophagy-like responses, such as swollen cell morphology, empty cytoplasm, acidic vesicles, and LC3-II accumulation, in an oral cancer cell line, OECM-1. To further assess the responses of other cell types to ANE 30–100K, we used both normal and malignant cells as the targets of ANE 30–100K and found that normal oral fibroblasts (CMT415), peripheral blood lymphocytes (PBLs), Jurkat leukemia T cells, and esophageal carcinoma cells (CE81T/VGH) exhibited similar responses after ANE 30–100K challenge. ANE 30–100K drastically increased acidic vesicle-containing PBLs isolated from two independent donors (from 0.1% to 92.1% and 2.9% to 64.2%). Furthermore, both ANE- and ANE 30–100K-induced LC3-II accumulation in CMT415 and CE81T/VGH was further increased in the presence of the lysosomal protease inhibitors (pepstatin A, E64d, and leupeptin). On the other hand, ANE 30–100K also increased the level of intracellular reactive oxygen species (ROS), and the ROS scavengers, N-acetylcysteine (NAC) and Tiron, inhibited ANE 30–100K-induced cell death and LC3-II accumulation. Collectively, these results suggest the existence of an autophagy-inducing AN ingredient (AIAI) in ANE 30–100K, which renders ANE as an autophagic flux inducer through ROS in both normal and malignant cells.
Relation:	Oral Oncology 46(11)：p.822-828
Appears in Collections:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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