scholarly journals Biliverdin’s regulation of reactive oxygen species signalling leads to potent inhibition of proliferative and angiogenic pathways in head and neck cancer

2014 ◽  
Vol 110 (8) ◽  
pp. 2116-2122 ◽  
Author(s):  
J Zheng ◽  
D A Nagda ◽  
S A Lajud ◽  
S Kumar ◽  
A Mouchli ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Potent Inhibition

scholarly journals Reactive oxygen species and p21Waf1/Cip1 are both essential for p53-mediated senescence of head and neck cancer cells

2015 ◽  
Vol 6 (3) ◽  
pp. e1678-e1678 ◽  
Author(s):  
A L Fitzgerald ◽  
A A Osman ◽  
T-X Xie ◽  
A Patel ◽  
H Skinner ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Cancer Cells ◽  
Neck Cancer ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Head and Neck Cancer Cell Death due to Mitochondrial Damage Induced by Reactive Oxygen Species from Nonthermal Plasma-Activated Media: Based on Transcriptomic Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Chan Oh ◽  
Ho-Ryun Won ◽  
Woo Seok Kang ◽  
Dae-Woong Kim ◽  
Seung-Nam Jung ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Head And Neck Cancer ◽  
Targeted Therapy ◽  
Head And Neck ◽  
Neck Cancer ◽  
Nonthermal Plasma ◽  
Mitochondrial Damage ◽  
Oxygen Species ◽  
Anticancer Effects

Mitochondrial targeted therapy is a next-generation therapeutic approach for cancer that is refractory to conventional treatments. Mitochondrial damage caused by the excessive accumulation of reactive oxygen species (ROS) is a principle of mitochondrial targeted therapy. ROS in nonthermal plasma-activated media (NTPAM) are known to mediate anticancer effects in various cancers including head and neck cancer (HNC). However, the signaling mechanism of HNC cell death via NTPAM-induced ROS has not been fully elucidated. This study evaluated the anticancer effects of NTPAM in HNC and investigated the mechanism using transcriptomic analysis. The viability of HNC cells decreased after NTPAM treatment due to enhanced apoptosis. A human fibroblast cell line and three HNC cell lines were profiled by RNA sequencing. In total, 1 610 differentially expressed genes were identified. Pathway analysis showed that activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) were upstream regulators. Mitochondrial damage was induced by NTPAM, which was associated with enhancements of mitochondrial ROS (mtROS) and ATF4/CHOP regulation. These results suggest that NTPAM induces HNC cell death through the upregulation of ATF4/CHOP activity by damaging mitochondria via excessive mtROS accumulation, similar to mitochondrial targeted therapy.

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