Programmed cell death, redox imbalance, and cancer therapeutics

Dai, Xiaofeng; Wang, Danjun; Zhang, Jianying

doi:10.1007/s10495-021-01682-0

Cited by 40 publications

(23 citation statements)

References 528 publications

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“…Our data indicate the induction of programmed cell death upon plasma treatment rather than necrotic cell death. This is in line with other publications [ 57 , 58 ]. The inhibition of cell death by adding NAC and/or catalase shows that ROS are the main effectors.…”

Section: Discussionsupporting

confidence: 94%

Toxicity and virucidal activity of a neon-driven micro plasma jet on eukaryotic cells and a coronavirus

Mrochen

Miebach

Skowski

et al. 2022

Free Radical Biology and Medicine

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Section: Discussionsupporting

confidence: 94%

Toxicity and virucidal activity of a neon-driven micro plasma jet on eukaryotic cells and a coronavirus

Mrochen

Miebach

Skowski

et al. 2022

Free Radical Biology and Medicine

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“…Apoptosis is a major type of programmed cell death. Apoptosis is characterized as the formation of apoptotic bodies and DNA fragmentation [ 17 ]. In colorectal cancer SW-620 cells, shikonin promoted galectin-1 dimerization and triggered apoptosis in a ROS-dependent manner [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells

Tsai¹,

Shih

Ong

et al. 2021

Antioxidants

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Shikonin mitigated tumor cell proliferation by elevating reactive oxygen species (ROS) levels. Herein, we investigated the effects of shikonin on renal cancer cell (RCC) cell proliferation. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that shikonin dose-dependently reduced the proliferation of Caki-1 and ACHN cells. Shikonin remarkably triggered necrosis and apoptosis in Caki-1 and ACHN cells in proportion to its concentration. Moreover, necrostatin-1 recovered cell viability in the presence of shikonin. Elevated ROS levels and mitochondrial dysfunction were also found in shikonin treatment groups. Pretreatment with N-acetyl cysteine remarkably mitigated shikonin-induced cell death and ROS generation. Western blot analysis revealed that shikonin reduced pro-PARP, pro-caspase-3, and Bcl-2 expression and increased cleavage PARP expression. Enhanced autophagy was also found in the shikonin-treated group as evidenced by acridine orange staining. Moreover, light chain 3B (LC3B)-II accumulation and enhanced p62 expression indicated that autophagy occurred in the shikonin-treated group. LC3B knockdown considerably recovered cell viability in the presence of shikonin. Shikonin treatment elevated p38 activity in a dose-dependent manner. In conclusion, our results revealed that shikonin triggered programmed cell death via the elevation of ROS level and p38 activity in different types of RCC cells. These findings suggested that shikonin may be a potential anti-RCC agent.

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“…Redox imbalance has been indicated as a causal factor of a variety of disorders such as cancer (263)(264)(265) and hypertension (266) with translational significance. Besides, reactive oxygen and nitrogen species (RONS) are also important signaling molecules with known roles on normal function regulation such as insulin and growth factor signaling (267).…”

Section: Trends In Omics Technology Developmentmentioning

confidence: 99%

Advances and Trends in Omics Technology Development

2022

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The human history has witnessed the rapid development of technologies such as high-throughput sequencing and mass spectrometry that led to the concept of “omics” and methodological advancement in systematically interrogating a cellular system. Yet, the ever-growing types of molecules and regulatory mechanisms being discovered have been persistently transforming our understandings on the cellular machinery. This renders cell omics seemingly, like the universe, expand with no limit and our goal toward the complete harness of the cellular system merely impossible. Therefore, it is imperative to review what has been done and is being done to predict what can be done toward the translation of omics information to disease control with minimal cell perturbation. With a focus on the “four big omics,” i.e., genomics, transcriptomics, proteomics, metabolomics, we delineate hierarchies of these omics together with their epiomics and interactomics, and review technologies developed for interrogation. We predict, among others, redoxomics as an emerging omics layer that views cell decision toward the physiological or pathological state as a fine-tuned redox balance.

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Programmed cell death, redox imbalance, and cancer therapeutics

Cited by 40 publications

References 528 publications

Toxicity and virucidal activity of a neon-driven micro plasma jet on eukaryotic cells and a coronavirus

Toxicity and virucidal activity of a neon-driven micro plasma jet on eukaryotic cells and a coronavirus

Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells

Advances and Trends in Omics Technology Development

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