Imatinib mesylate induction of ROS-dependent apoptosis in melanoma B16F0 cells

Chang, Shao Ping; Shen, Shing Chuan; Lee, William R.; Yang, Lingling; Chen, Yen Chou

doi:10.1016/j.jdermsci.2011.03.001

Cited by 42 publications

(26 citation statements)

References 35 publications

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“…However, auranofin, a gold-containing chemical applied for treatment of rheumatoid arthritis, inhibits thioredoxin reductase, inducing ROS formation and in this way dramatically inhibiting GIST cell growth, and it also induces apoptosis in imatinib-resistant cells [60]. ROS-dependent apoptosis has also been reported in melanoma cell lines after imatinib treatment [61]. …”

Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

Reactive Oxygen Species‐Mediated Mechanisms of Action of Targeted Cancer Therapy

Teppo

Soini

Karihtala

2017

Oxidative Medicine and Cellular Longevity

137

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Targeted cancer therapies, involving tyrosine kinase inhibitors and monoclonal antibodies, for example, have recently led to substantial prolongation of survival in many metastatic cancers. Compared with traditional chemotherapy and radiotherapy, where reactive oxygen species (ROS) have been directly linked to the mediation of cytotoxic effects and adverse events, the field of oxidative stress regulation is still emerging in targeted cancer therapies. Here, we provide a comprehensive review regarding the current evidence of ROS-mediated effects of antibodies and tyrosine kinase inhibitors, use of which has been indicated in the treatment of solid malignancies and lymphomas. It can be concluded that there is rapidly emerging evidence of ROS-mediated effects of some of these compounds, which is also relevant in the context of drug resistance and how to overcome it.

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Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

Reactive Oxygen Species‐Mediated Mechanisms of Action of Targeted Cancer Therapy

Teppo

Soini

Karihtala

2017

Oxidative Medicine and Cellular Longevity

137

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“…Cellular ROS can be generated either through the process of mitochondrial oxidative phosphorylation or upon challenge by exogenous factors, including bacteria and their virulence factors (7,8). Overwhelming ROS activity, caused by either an increase in ROS levels or a decrease in antioxidant capacity, induces oxidative stress and results in collateral damage to nucleic acids, proteins, and lipids (9,10). In contrast, restrained ROS production plays an important role in microbial host defense, as ROS can regulate diverse signaling pathways and consequently modify inflammatory responses (11,12).…”

mentioning

confidence: 99%

Porphyromonas gingivalis-Induced Reactive Oxygen Species Activate JAK2 and Regulate Production of Inflammatory Cytokines through c-Jun

et al. 2014

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Pathogen-induced reactive oxygen species (ROS) play a crucial role in host innate immune responses through regulating the quality and quantity of inflammatory mediators. However, the underlying molecular mechanisms of this effect have yet to be clarified. In this study, we examined the mechanism of action of ROS stimulated by Porphyromonas gingivalis in gingival epithelial cells. P. gingivalis induced the rapid production of ROS, which lead to the phosphorylation of JAK2 and increased levels of secreted proinflammatory cytokines interleukin-6 (IL-6) and IL-1␤. Neutralization of ROS by N-acetyl-L-cysteine (NAC) abrogated the phosphorylation of JAK2 and suppressed the production of IL-6 and IL-1␤. ROS-mediated phosphorylation of JAK2 induced the phosphoactivation of c-Jun amino-terminal protein kinase (JNK) and the downstream transcriptional regulator c-Jun. Inhibition of JAK2, either pharmacologically or by small interfering RNA (siRNA), reduced both the phosphorylation of these molecules and the production of proinflammatory cytokines in response to P. gingivalis. Furthermore, pharmacological inhibition or siRNA-mediated gene silencing of JNK or c-Jun mimicked the effect of JAK2 inhibition to suppress P. gingivalisinduced IL-6 and IL-1␤ levels. The results show that ROS-mediated activation of JAK2 is required for P. gingivalis-induced inflammatory cytokine production and that the JNK/c-Jun signaling axis is involved in the ROS-dependent regulation of IL-1␤ and IL-6 production.

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“…The JNK pathway was found to mediate doxycycline-induced cell death via ROS generation and apoptosis signal-regulating kinase 1 (ASK1) activation in A2058 melanoma cells (Shieh et al, 2010). Imatinib mesylate, a RTK inhibitor, mediated apoptosis and induced high levels of phospho-JNK and p38 in B16F0 melanoma cells (Chang et al, 2011). In this study, SP600125 was shown to enhance apoptosis in the imatinib mesylate-treated melanoma cells.…”

Section: P38 Mapk and Jnkmentioning

confidence: 65%