Silver nanoparticles induce apoptosis via NOX4-derived mitochondrial reactive oxygen species and endoplasmic reticulum stress in colorectal cancer cells

被引：12

作者：

Quan, Juan-Hua ^{[1
]}

Gao, Fei Fei ^{[2
,3
,4
]}

Chu, Jia-Qi ^{[5
]}

Cha, Guang-Ho ^{[3
,4
]}

Yuk, Jae-Min ^{[2
,3
,4
]}

Wu, Weiyun ^{[1
]}

Lee, Young-Ha ^{[2
,3
,4
]}

机构：

[1] Guangdong Med Univ, Dept Gastroenterol, Affiliated Hosp, Zhanjiang 524001, Peoples R China

[2] Chungnam Natl Univ, Brain Korea 21 Four Project Med Sci, Daejeon 35015, South Korea

[3] Chungnam Natl Univ, Dept Med Sci, Coll Med, Daejeon 35015, South Korea

[4] Chungnam Natl Univ, Dept Infect Biol, Coll Med, Daejeon 35015, South Korea

[5] Guangdong Med Univ, Stem Cell Res & Cellular Therapy Ctr, Affiliated Hosp, Zhanjiang 524001, Peoples R China

来源：

NANOMEDICINE | 2021年 / 16卷 / 16期

基金：

中国国家自然科学基金; 新加坡国家研究基金会;

关键词：

apoptosis; colorectal cancer; ER stress; NOX4; reactive oxygen species; silver nanoparticles; xenograft nude mice; IN-VITRO; DEATH;

D O I：

10.2217/nnm-2021-0098

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Aim: To investigate the anticancer mechanisms of silver nanoparticles (AgNPs) in colorectal cancer. Methods: Anticancer effects of AgNPs were determined in colorectal cancer HCT116 cells and xenograft mice using cellular and molecular methods. Results: AgNPs induced mitochondrial reactive oxygen species production, mitochondrial dysfunction and endoplasmic reticulum (ER) stress responses through NOX4 and led to HCT116 cell apoptosis. Pretreatment with DPI or 4-PBA significantly inhibited mitochondrial reactive oxygen species production, apoptosis, ER stress response, NOX4 expression and mitochondrial dysfunction in AgNP-treated HCT116 cells. AgNPs also significantly suppressed HCT116 cell-based xenograft tumor growth in nude mice by inducing apoptosis and ER stress responses. Conclusion: AgNPs exert anticancer effects against colorectal cancer via ROS- and ER stress-related mitochondrial apoptosis pathways.

引用

页码：1357 / 1375

页数：19

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