scholarly journals GDF15 contributes to radioresistance and cancer stemness of head and neck cancer by regulating cellular reactive oxygen species via a SMAD-associated signaling pathway

Oncotarget ◽  
2016 ◽  
Vol 8 (1) ◽  
pp. 1508-1528 ◽  
Author(s):  
Yan-Liang Li ◽  
Joseph T. Chang ◽  
Li-Yu Lee ◽  
Kang-Hsing Fan ◽  
Ya-Ching Lu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Signaling Pathway ◽  
Neck Cancer ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cancer Stemness ◽  
Cellular Reactive Oxygen Species

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.

scholarly journals Reactive oxygen species rescue regeneration after silencing the MAPK–ERK signaling pathway in Schmidtea mediterranea

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
V. Jaenen ◽  
S. Fraguas ◽  
K. Bijnens ◽  
M. Heleven ◽  
T. Artois ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Light Therapy ◽  
Erk Signaling ◽  
Model Organisms ◽  
Ros Production ◽  
Oxygen Species ◽  
Planarian Regeneration ◽  
Egfr Signaling Pathway

AbstractDespite extensive research on molecular pathways controlling the process of regeneration in model organisms, little is known about the actual initiation signals necessary to induce regeneration. Recently, the activation of ERK signaling has been shown to be required to initiate regeneration in planarians. However, how ERK signaling is activated remains unknown. Reactive Oxygen Species (ROS) are well-known early signals necessary for regeneration in several models, including planarians. Still, the probable interplay between ROS and MAPK/ERK has not yet been described. Here, by interfering with major mediators (ROS, EGFR and MAPK/ERK), we were able to identify wound-induced ROS, and specifically H2O2, as upstream cues in the activation of regeneration. Our data demonstrate new relationships between regeneration-related ROS production and MAPK/ERK activation at the earliest regeneration stages, as well as the involvement of the EGFR-signaling pathway. Our results suggest that (1) ROS and/or H2O2 have the potential to rescue regeneration after MEK-inhibition, either by H2O2-treatment or light therapy, (2) ROS and/or H2O2 are required for the activation of MAPK/ERK signaling pathway, (3) the EGFR pathway can mediate ROS production and the activation of MAPK/ERK during planarian regeneration.

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