An Isoquinolin-1(2H )-Imine Derivative Induces Cell Death via Generation of Reactive Oxygen Species and Activation of JNK in Human A549 Cancer Cells

2017 ◽  
Vol 118 (12) ◽  
pp. 4394-4403
Author(s):  
Jing Liu ◽  
Tongyang Liu ◽  
Hanchuan Mou ◽  
Shuting Jia ◽  
Chao Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Human A549

Mitochondrion-targeted selenium nanoparticles enhance reactive oxygen species-mediated cell death

Nanoscale ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 1389-1396 ◽  
Author(s):  
Yuan Zhuang ◽  
Longjie Li ◽  
Liandong Feng ◽  
Shuangshuang Wang ◽  
Huimin Su ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Selenium Nanoparticles ◽  
Oxygen Species ◽  
Targeting Ability ◽  
Mitochondria Targeting

Selenium nanoparticles (SeNPs) with mitochondria targeting ability can significantly enhance the reactive oxygen species (ROS) induced cell death in cancer cells, while remaining less toxic in healthy cells.

JLP-JNK signaling protects cancer cells from reactive oxygen species-induced cell death

2018 ◽  
Vol 501 (3) ◽  
pp. 724-730 ◽  
Author(s):  
Rong Li ◽  
I. Ketut Gunarta ◽  
Ryusuke Suzuki ◽  
Jambaldorj Boldbaatar ◽  
Ryota Nakazato ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Jnk Signaling

scholarly journals Reactive Oxygen Species Mediate 6c-Induced Mitochondrial and Lysosomal Dysfunction, Autophagic Cell Death, and DNA Damage in Hepatocellular Carcinoma

2021 ◽  
Vol 22 (20) ◽  
pp. 10987
Author(s):  
Senzhen Wang ◽  
Xiaojuan Xu ◽  
Delu Che ◽  
Ronghui Fan ◽  
Mengke Gao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Comparative Proteomics ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Lysosomal Dysfunction ◽  
Mitochondrial Ros

Increasing the level of reactive oxygen species (ROS) in cancer cells has been suggested as a viable approach to cancer therapy. Our previous study has demonstrated that mitochondria-targeted flavone-naphthalimide-polyamine conjugate 6c elevates the level of ROS in cancer cells. However, the detailed role of ROS in 6c-treated cancer cells is not clearly stated. The biological effects and in-depth mechanisms of 6c in cancer cells need to be further investigated. In this study, we confirmed that mitochondria are the main source of 6c-induced ROS, as demonstrated by an increase in 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and MitoSox fluorescence. Compound 6c-induced mitochondrial ROS caused mitochondrial dysfunction and lysosomal destabilization confirmed by absolute quantitation (iTRAQ)-based comparative proteomics. Compound 6c-induced metabolic pathway dysfunction and lysosomal destabilization was attenuated by N-acetyl-L-cysteine (NAC). iTRAQ-based comparative proteomics showed that ROS regulated the expression of 6c-mediated proteins, and treatment with 6c promoted the formation of autophagosomes depending on ROS. Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and γH2A.X, which was diminished by pretreatment with NAC. Compound 6c-induced cell death was partially reversed by 3-methyladenine (3-MA), bafilomycin (BAF) A1, and NAC, respectively. Taken together, the data obtained in our study highlighted the involvement of mitochondrial ROS in 6c-induced autophagic cell death, mitochondrial and lysosomal dysfunction, and DNA damage.

Fructose‐1,6‐bisphosphate induces generation of reactive oxygen species and activation of p53‐dependent cell death in human endometrial cancer cells

2020 ◽  
Author(s):  
Bruna Pasqualotto Costa ◽  
Marcella Tornquist Nassr ◽  
Fernando Mendonça Diz ◽  
Leonardo Pfeiff Carlessi ◽  
Krist Helen Antunes Fernandes ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Endometrial Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dependent Cell ◽  
Fructose 1,6 Bisphosphate
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