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Knockdown of TWIST1 enhances arsenic trioxide- and ionizing radiation-induced cell death in lung cancer cells by promoting mitochondrial dysfunction

Authors
 Sung-Keum Seo  ;  Jae-Hee Kim  ;  Ha-Na Choi  ;  Tae-Boo Choe  ;  Seok-Il Hong  ;  Jae-Youn Yi  ;  Sang-Gu Hwang  ;  Hyun-Gyu Lee  ;  Yun-Han Lee  ;  In-Chul Park 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.449(4) : 490-495, 2014 
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN
 0006-291X 
Issue Date
2014
MeSH
Acetylcysteine/pharmacology ; Arsenicals ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Non-Small-Cell Lung/radiotherapy ; Cell Death/drug effects ; Cell Death/radiation effects ; Gene Knockdown Techniques ; Humans ; Membrane Potential, Mitochondrial/drug effects ; Nuclear Proteins/biosynthesis ; Nuclear Proteins/genetics* ; Oxides ; RNA, Small Interfering/pharmacology ; Radiation, Ionizing ; Reactive Oxygen Species/metabolism ; Twist-Related Protein 1/biosynthesis ; Twist-Related Protein 1/genetics*
Keywords
Arsenic trioxide ; Irradiation ; Mitochondria dysfunction ; Reactive oxygen species ; TWIST1
Abstract
TWIST1 is implicated in the process of epithelial mesenchymal transition, metastasis, stemness, and drug resistance in cancer cells, and therefore is a potential target for cancer therapy. In the present study, we found that knockdown of TWIST1 by small interfering RNA (siRNA) enhanced arsenic trioxide (ATO)- and ionizing radiation (IR)-induced cell death in non-small-cell lung cancer cells. Interestingly, intracellular reactive oxygen species levels were increased in cells treated with TWIST1 siRNA and further increased by co-treatment with ATO or IR. Pretreatment of lung cancer cells with the antioxidant N-acetyl-cysteine markedly suppressed the cell death induced by combined treatment with TWIST1 siRNA and ATO or IR. Moreover, treatment of cells with TWIST1 siRNA induced mitochondrial membrane depolarization and significantly increased mitochondrial fragmentation (fission) and upregulated the fission-related proteins FIS1 and DRP1. Collectively, our results demonstrate that siRNA-mediated TWIST1 knockdown induces mitochondrial dysfunction and enhances IR- and ATO-induced cell death in lung cancer cells.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X14008845
DOI
10.1016/j.bbrc.2014.05.030
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
Yonsei Authors
Lee, Yun Han(이윤한)
Lee, Hyun Gyu(이현규)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99272
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