JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells

Qiu, Mingning; Chen, Lieqian; Tan, Guobin; Ke, Longzhi; Zhang, Sai; Chen, Hege; Liu, Jianjun

doi:10.3892/ol.2016.5535

Cited by 20 publications

(28 citation statements)

References 14 publications

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“…A number of researchers noted that excessive ROS was the cause of apoptosis. [35][36][37][38] Daniel et al found that the death of bacteria induced by antibiotics displayed the same physiological and biochemical characteristics as apoptosis. 39 Other scholars also observed the morphological changes and biochemical reactions related to apoptosis in prokaryotes.…”

Section: Discussionmentioning

confidence: 99%

Antibacterial activity and mechanism of silver nanoparticles against multidrug-resistant Pseudomonas aeruginosa

Liao¹,

Zhang²,

Pan³

et al. 2019

IJN

377

203

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Background: The threat of drug-resistant Pseudomonas aeruginosa requires great efforts to develop highly effective and safe bactericide. Objective: This study aimed to investigate the antibacterial activity and mechanism of silver nanoparticles (AgNPs) against multidrug-resistant P. aeruginosa. Methods: The antimicrobial effect of AgNPs on clinical isolates of resistant P. aeruginosa was assessed by minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC). In multidrug-resistant P. aeruginosa, the alterations of morphology and structure were observed by the transmission electron microscopy (TEM); the differentially expressed proteins were analyzed by quantitative proteomics; the production of reactive oxygen species (ROS) was assayed by H 2 DCF-DA staining; the activity of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) was chemically measured and the apoptosis-like effect was determined by flow cytometry. Results: Antimicrobial tests revealed that AgNPs had highly bactericidal effect on the drug-resistant or multidrug-resistant P. aeruginosa with the MIC range of 1.406-5.625 µg/mL and the MBC range of 2.813-5.625 µg/mL. TEM showed that AgNPs could enter the multidrug-resistant bacteria and impair their morphology and structure. The proteomics quantified that, in the AgNP-treated bacteria, the levels of SOD, CAT, and POD, such as alkyl hydroperoxide reductase and organic hydroperoxide resistance protein, were obviously high, as well as the significant upregulation of low oxygen regulatory oxidases, including cbb3-type cytochrome c oxidase subunit P2, N2, and O2. Further results confirmed the excessive production of ROS. The antioxidants, reduced glutathione and ascorbic acid, partially antagonized the antibacterial action of AgNPs. The apoptosis-like rate of AgNP-treated bacteria was remarkably higher than that of the untreated bacteria (P,0.01). Conclusion: This study proved that AgNPs could play antimicrobial roles on the multidrug-resistant P. aeruginosa in a concentration-and time-dependent manner. The main mechanism involves the disequilibrium of oxidation and antioxidation processes and the failure to eliminate the excessive ROS.

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Section: Discussionmentioning

confidence: 99%

Antibacterial activity and mechanism of silver nanoparticles against multidrug-resistant Pseudomonas aeruginosa

Liao¹,

Zhang²,

Pan³

et al. 2019

IJN

377

203

View full text Add to dashboard Cite

show abstract

“…Conversely, there are several reports on the relationship between ROS production and treatment efficacy in prostate cancer. For example, treatment with JS-K, a glutathione S transferase-activated nitric oxide donor prodrug, for 24 h, increased the proportion of apoptotic cells, by inducing ROS production in prostate cancer cells (22RV1, C4-2, LNCaP, and PC-3) [ 140 ]. Interestingly, these authors also showed that the pro-apoptotic effect of JS-K is dose-dependent, and 22RV1 and C4-2 cells were more sensitive than LNCaP and PC-3 cells [ 141 ].…”

Section: Apoptosis and Rosmentioning

confidence: 99%

A Mini-Review of Reactive Oxygen Species in Urological Cancer: Correlation with NADPH Oxidases, Angiogenesis, and Apoptosis

Miyata

Matsuo

Sagara

et al. 2017

IJMS

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Oxidative stress refers to elevated reactive oxygen species (ROS) levels, and NADPH oxidases (NOXs), which are one of the most important sources of ROS. Oxidative stress plays important roles in the etiologies, pathological mechanisms, and treatment strategies of vascular diseases. Additionally, oxidative stress affects mechanisms of carcinogenesis, tumor growth, and prognosis in malignancies. Nearly all solid tumors show stimulation of neo-vascularity, termed angiogenesis, which is closely associated with malignant aggressiveness. Thus, cancers can be seen as a type of vascular disease. Oxidative stress-induced functions are regulated by complex endogenous mechanisms and exogenous factors, such as medication and diet. Although understanding these regulatory mechanisms is important for improving the prognosis of urothelial cancer, it is not sufficient, because there are controversial and conflicting opinions. Therefore, we believe that this knowledge is essential to discuss observations and treatment strategies in urothelial cancer. In this review, we describe the relationships between members of the NOX family and tumorigenesis, tumor growth, and pathological mechanisms in urological cancers including prostate cancer, renal cell carcinoma, and urothelial cancer. In addition, we introduce natural compounds and chemical agents that are associated with ROS-induced angiogenesis or apoptosis.

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“…Reactive oxygen species (ROS) play essential roles in maintaining biological functions such as cell proliferation and apoptosis [ 17 ]. The moderation of intracellular ROS levels can promote cell proliferation and differentiation, and the overproduction of ROS can lead to cytotoxicity in cancer cells [ 18 , 19 ]. There is evidence that MAPK and STAT3 are representative ROS-responsive signaling pathways that are involved in mitochondrial dysfunction and cell survival [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Quinalizarin Induces Apoptosis through Reactive Oxygen Species (ROS)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathways in Colorectal Cancer Cells

Wang

Luo

et al. 2018

Med Sci Monit

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BackgroundQuinalizarin (1,2,5,8-tetrahydroxyanthraquinone) exhibits potentially useful anticancer effects by inducing apoptosis in several types of cancer, but its underlying mechanism of action remains unknown. The present study examined the effects of quinalizarin on the induction of cell cycle arrest, apoptosis, the generation of reactive oxygen species (ROS), other underlying mechanisms, and its role in modifying colorectal cancer cell lines.Material/MethodsThe MTT assay was used to evaluate the viability of SW480 and HCT-116 cells that had been treated with quinalizarin and 5-fluorouracil (5-FU). Cell cycle arrest and apoptosis were analyzed by flow cytometry. Western blotting was used to investigate the mitochondrial pathway; Akt, MAPK, and STAT3 signaling pathways were also investigated. The relationship between ROS generation and apoptosis was analyzed by flow cytometry and western blotting.ResultsThe results indicated that quinalizarin significantly inhibits the viability of SW480 and HCT-116 cells in a dose-dependent manner. Quinalizarin induced SW480 cell cycle arrest at G2/M by regulating cyclin B1 and CDK1/2. The apoptosis-related protein expression levels of p-p53, Bad, cleaved caspase-3, cleaved PARP and p-JNK were increased in quinalizarin-treated cells, while protein expression levels Bcl-2, p-Akt, p-ERK, and p-STAT3 were decreased. Quinalizarin induced apoptosis in colorectal cancer cells by regulating MAPK and STAT3 signaling pathways via ROS generation.ConclusionsQuinalizarin induces apoptosis via ROS-mediated MAPK/STAT3 signaling pathways.

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JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells

Cited by 20 publications

References 14 publications

<p>Antibacterial activity and mechanism of silver nanoparticles against multidrug-resistant <em>Pseudomonas aeruginosa</em></p>

<p>Antibacterial activity and mechanism of silver nanoparticles against multidrug-resistant <em>Pseudomonas aeruginosa</em></p>

A Mini-Review of Reactive Oxygen Species in Urological Cancer: Correlation with NADPH Oxidases, Angiogenesis, and Apoptosis

Quinalizarin Induces Apoptosis through Reactive Oxygen Species (ROS)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathways in Colorectal Cancer Cells

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