Ad5-EMC6 mediates antitumor activity in gastric cancer cells through the mitochondrial apoptosis pathway.

作者: Riyong Li , Xiaokun Wang , Xuan Zhang , Jiahong Yu , Jinqiu Feng

DOI: 10.1016/J.BBRC.2019.04.023

关键词:

摘要: Endoplasmic reticulum membrane protein complex subunit 6 (EMC6), also known as transmembrane 93 (transmembrane 93, TMEM93), is an autophagy-related protein. EMC6 overexpression inhibits cancer cell growth and induces apoptosis, but the interaction partners of its cellular responsibilities remain incompletely understood. In this study, we report that adenovirus-mediated ectopic (Ad5-EMC6) in BGC823 SGC7901 gastric cells decreases activity ERK1/2, down-regulates levels BCL-2 phosphorylated BCL-2, increases expression tBID BAX, mitochondrial potential subsequently leading to apoptosis. a xenograft tumor model, found Ad5-EMC6 impairs tumorigenesis nude mice. Additionally, enhances sensitivity chemotherapeutic drug etoposide. Collectively, these results demonstrate EMC6-induced apoptosis occurs at least partially through mitochondrial-mediated pathway. Our study suggests rational basis for clinical application cancer.

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