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

Abstract

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.

Porcine epidemic diarrhea virus infections induce apoptosis in Vero cells via a reactive oxygen species (ROS)/p53, but not p38 MAPK and SAPK/JNK signalling pathways

“…Cells maintain a balance of ROS by means of the antioxidant system in physiological conditions (Torres et al, 2006). However, triggered by stress stimuli such as ionising radiation, chemotherapeutic drugs and viral infections, ROS can be excessively accumulated and regulate several pathological processes including proliferation, inflammation, autophagy and apoptosis (Circu and Aw, 2010;Miyata et al, 2017). Several studies showed that ROS participate in apoptosis induced by viruses.…”

Copper(II) complexes of coumarin-derived Schiff base ligands: Pro- or antioxidant activity in MCF-7 cells?

“…1,2 However, uncontrolled generation of ROS as well as reactive nitrogen species (RNS) have been implicated in many diseases including cardiovascular disease, 3 arthritis, 4 neurodegenerative disease 5 and cancer. 6 With respect to cancer, ROS have been shown to be present at high concentrations in some types of cancers, due to the high metabolic activity of the cells. 7 ROS can cause modification of base pairs through abstraction or addition of hydrogen, induction of DNA strand breaks and DNA cross-linking causing DNA mutagenesis and initiating uncontrolled division, the initial step in tumour development.…”

“…7 ROS can cause modification of base pairs through abstraction or addition of hydrogen, induction of DNA strand breaks and DNA cross-linking causing DNA mutagenesis and initiating uncontrolled division, the initial step in tumour development. 6 However, numerous studies have also concluded that increasing ROS levels can promote oxidative stress-induced cancer cell death. 8 Thus while the role of ROS in the prevention/induction of cancer is a topic of intense debate in general, the idea of using therapies which selectively generate oxidative stress in cancer cells was proposed as a possible therapeutic treatment for malignant cancers.…”

“…A series of copper(II) complexes of Schiff base-derived ligands (1)(2)(3)(4)(5)(6)(7) were studied for their pro-and antioxidant behaviour in the MCF-7 human breast cancer cell line. The coordination modes of two of the copper(II) complexes were investigated by pH-potentiometry, EPR and UV-Vis spectroscopic methods.…”

ERβ and NFκB—Modulators of Zearalenone-Induced Oxidative Stress in Human Prostate Cancer Cells

“…Oxidative stress in cancer cells plays a dual role: the generation of reactive oxygen species (ROS) in cells increases the proliferation and migration of cells and participates in the initiation and progression of PCa [1], but on the other hand, excessive ROS production induces DNA damage and triggers apoptosis [2]. Nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB) signaling pathway is believed to be a link between inflammation and cancer, due to the induction of proliferation, blocking apoptosis in cells and maintaining angiogenesis [3], and the induction of oxidative stress with hypoxia inducible factor 1 alpha (HIF-1α) and estrogen receptor β (ERβ) [4].…”