scholarly journals The quinone-based derivative, HMNQ induces apoptotic and autophagic cell death by modulating reactive oxygen species in cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (59) ◽  
pp. 99637-99648 ◽  
Author(s):  
Eun Byul Lee ◽  
Min Gyeong Cheon ◽  
Jun Cui ◽  
Yoo Jin Lee ◽  
Eun Kyoung Seo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Autophagic Cell Death ◽  
Oxygen Species

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.

scholarly journals Parthenolide Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in Human Osteosarcoma Cells

2016 ◽  
Vol 40 (1-2) ◽  
pp. 146-154 ◽  
Author(s):  
Chen Yang ◽  
Qing Ou Yang ◽  
Qing-Jie Kong ◽  
Wen Yuan ◽  
Yue-Ping Ou Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Pharmacological Action ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Background and Aim: Osteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Parthenolide, a naturally occurring small molecule that interferes with NF-κB signaling, has recently attracted considerable attention because of its pharmacological action involving anti-cancer effects. However, the mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. Methods: In this study, the effects of parthenolide were evaluated and characterized in human osteosarcoma cancer cell. Cell viability was assessed by CCK-8. Apoptosis was assessed by Annexin V-FITC/PI Flow cytometry assay. Relative quantitative real-time PCR and western blot were used to determine the expressions of genes and proteins. Results: Our results suggest that parthenolide did not cause caspase-dependent cell death in osteosarcoma cancer cells, as indicated by the absence of significant early apoptosis as well as caspase-3 cleavage. Instead, parthenolide increased the autophagy and mitophagy, as characterized by increased PINK1 and Parkin translocation to mitochondria and enhanced autophagy proteins. The induction of autophagy by parthenolide was associated with the increase of reactive oxygen species (ROS). ROS antioxidants N-acetylcysteine (NAC) attenuated parthenolide-induced autophagy activity. Conclusions: Our findings unveil a novel mechanism of drug action by parthenolide in osteosarcoma cancer cells and suggest a potential value of treating osteosarcoma cancer through a caspase-independent autophagic cell death by ROS activation.

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

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
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