Sensitization of melanoma cells to alkylating agent-induced DNA damage and cell death via orchestrating oxidative stress and IKKβ inhibition

Tse, Anfernee Kai-Wing; Chen, Ying‐Jie; Fu, Xiu‐Qiong; Su, Tao; Li, Ting; Guo, Hui; Zhu, Peili; Kwan, Hiu Yee; Cheng, Brian Chi‐Yan; Cao, Hongxin; Lee, Sally Kin-Wah; Fong, Wang‐Fun; Yu, Zhi‐Ling

doi:10.1016/j.redox.2017.01.010

Cited by 31 publications

(21 citation statements)

References 50 publications

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“…The hypothesis that NF‐κB activation produces an inflammatory response is derived from macrophage activation after NF‐κB hyperactivity . This is supported by the fact that numerous NF‐κB target genes are pro‐inflammatory, such as MMP9, iNOS, and NLRP3, whereas others have been shown to induce intrinsic apoptosis via ROS and p38 . Indeed, stimulation of NF‐κB is followed by TNFα activation, known to provoke apoptosis.…”

Section: Pathophysiology Of Cardiac Ir Injurymentioning

confidence: 99%

Protective role of melatonin in cardiac ischemia‐reperfusion injury: From pathogenesis to targeted therapy

Zhou

Zhu

et al. 2018

Journal of Pineal Research

202

133

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Acute myocardial infarction (MI) is a major cause of mortality and disability worldwide. In patients with MI, the treatment option for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PCI). However, the procedure of reperfusion itself induces cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. Recent evidence has depicted a promising role of melatonin, which possesses powerful antioxidative and anti‐inflammatory properties, in the prevention of ischemia‐reperfusion (IR) injury and the protection against cardiomyocyte death. A number of reports explored the mechanism of action behind melatonin‐induced beneficial effects against myocardial IR injury. In this review, we summarize the research progress related to IR injury and discuss the unique actions of melatonin as a protective agent. Furthermore, the possible mechanisms responsible for the myocardial benefits of melatonin against reperfusion injury are listed with the prospect of the use of melatonin in clinical application.

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Section: Pathophysiology Of Cardiac Ir Injurymentioning

confidence: 99%

Protective role of melatonin in cardiac ischemia‐reperfusion injury: From pathogenesis to targeted therapy

Zhou

Zhu

et al. 2018

Journal of Pineal Research

202

133

View full text Add to dashboard Cite

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“…Nevertheless, it was not found that Jinfukang induced apoptosis in lung cancer cells by intervening ROS pathway. Previous studies have confirmed that increased ROS levels can cause DNA damage and induce cell apoptosis [26]. Hence, we conducted research on this pathway and found that Jinfukang can significantly increase the levels of ROS in CTC-TJH-01 cells.…”

Section: Discussionmentioning

confidence: 74%

Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells

Que

Zhou

Luo

et al. 2019

BMC Complement Altern Med

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Background Metastasis is the main cause of lung cancer death. As a seed of metastasis, circulating tumor cells are an important target for metastasis intervention. The traditional Chinese medicine, Jinfukang, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). In this study, we investigated the action and underlying mechanisms of Jinfukang against circulating lung tumor cells. Methods The cell counting kit-8 (CCK-8), colony formation and cell cycle assays were used to study the cell proliferation ability. Flow cytometry was used to detect the apoptosis and the expression level of ROS and Caspase-3. Comet and TUNEL assays were used to detect DNA damage. DNA damage related pathway protein was detected by western blot. Results Jinfukang significantly inhibits the proliferation of CTC-TJH-01 cells by inducing G1 phase arrest and inhibits their colony formation in a dose-dependent manner. Moreover, Jinfukang induces apoptosis in CTC-TJH-01 cells through the ROS-mediated ATM/ATR-p53 pathway and DNA damage. Conclusions Our findings suggest that Jinfukang may be a potential drug for lung cancer metastasis. Electronic supplementary material The online version of this article (10.1186/s12906-019-2601-x) contains supplementary material, which is available to authorized users.

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“…Melanoma is a common malignant skin tumor with many different causes. As well-known, the oxidative stress and DNA damage caused by UV are the major causative factors of melanoma, while the involved molecular mechanism is still unclear (32–35). This study attempts to explain the molecular mechanism and screen new biomarkers.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-300: A Transcellular Mediator in Exosome Regulates Melanoma Progression

et al. 2019

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Melanoma is a common and high-mortality skin cancer. Oxidative stress and DNA damage caused by ultraviolet light (UV) are major causative factors of melanoma formation. However, the specific molecular mechanism is still unclear. In this study, 218 dysregulated genes and 104 dysregulated miRNAs in response to UV were screened by analyzing sequencing datasets. Among them, 29 up-regulated miRNAs and 28 down-regulated miRNAs were involved in the melanoma pathway. As the only differential gene in the melanoma pathway, GADD45B severely affects the prognosis of melanoma patients. MiR-300 is the only differentially expressed miRNA that regulates GADD45B. In addition, compared to normal melanocytes, miR-300 was significantly down-regulated in melanoma cells (log FC = −1.63) and exosomes (log FC = −1.34). Among the transcription factors predicted to regulate miR-300, MYC, PPARG, and ZIC2 were significantly up-regulated in melanoma cells, and TP53, JUN, JUNB, FOS, and FOSB interacted with GADD45B. We attempted to reveal the pathogenesis of melanoma and screen new biomarkers by constructing a TF-mRNA-miRNA axis in turn to provide a view for further research.

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Sensitization of melanoma cells to alkylating agent-induced DNA damage and cell death via orchestrating oxidative stress and IKKβ inhibition

Cited by 31 publications

References 50 publications

Protective role of melatonin in cardiac ischemia‐reperfusion injury: From pathogenesis to targeted therapy

Protective role of melatonin in cardiac ischemia‐reperfusion injury: From pathogenesis to targeted therapy

Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells

MicroRNA-300: A Transcellular Mediator in Exosome Regulates Melanoma Progression

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