Nitric oxide and interactions with reactive oxygen species in the development of melanoma, breast, and colon cancer: A redox signaling perspective

Monteiro, Hugo P.; Rodrigues, Elaine G.; Reis, Adriana Karla Cardoso Amorim; Longo, Luiz S.; Ogata, Fernando T.; Moretti, Ana Iochabel Soares; Costa, P.; Teodoro, Ana Caroline S.; Toledo, Mayte; Stern, Arnold

doi:10.1016/j.niox.2019.04.009

Cited by 66 publications

(35 citation statements)

References 177 publications

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“…NO does not destroy early steps of cell division in glycolytic cells because these bacteria obtain a sizable fraction of their purine nucleosides by favoring substrate-level phosphorylation and expressing enhanced IMPDH levels. Analogous glycolytic adaptations may provide a continuous supply of NTPs for undeterred growth of tumor cells despite a prevailing nitrosative environment (23). However, glycolysis is not sufficient to prevent growth arrest in bacteria undergoing nitrosative stress.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide disrupts bacterial cytokinesis by poisoning purine metabolism

et al. 2020

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Cytostasis is the most salient manifestation of the potent antimicrobial activity of nitric oxide (NO), yet the mechanism by which NO disrupts bacterial cell division is unknown. Here, we show that in respiring Escherichia coli, Salmonella, and Bacillus subtilis, NO arrests the first step in division, namely, the GTP-dependent assembly of the bacterial tubulin homolog FtsZ into a cytokinetic ring. FtsZ assembly fails in respiring cells because NO inactivates inosine 5′-monophosphate dehydrogenase in de novo purine nucleotide biosynthesis and quinol oxidases in the electron transport chain, leading to drastic depletion of nucleoside triphosphates, including the GTP needed for the polymerization of FtsZ. Despite inhibiting respiration and dissipating proton motive force, NO does not destroy Z ring formation and only modestly decreases nucleoside triphosphates in glycolytic cells, which obtain much of their ATP by substrate-level phosphorylation and overexpress inosine 5′-monophosphate dehydrogenase. Purine metabolism dictates the susceptibility of early morphogenic steps in cytokinesis to NO toxicity.

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Section: Discussionmentioning

confidence: 99%

Nitric oxide disrupts bacterial cytokinesis by poisoning purine metabolism

et al. 2020

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“…Gpx3 and Gpx8, two ROS scavengers and part of the glutathione peroxidase family that are crucial to maintain ROS levels at a certain range (Herault et al, 2012;Ramming et al, 2014), were progressively downregulated. On the other hand, Nos1, a member of the nitric oxide synthase family that synthesizes the reactive free radical nitric oxide (Liu et al, 2002;Monteiro et al, 2019), displayed a drastic increase in expression. Together, these results suggest that multiple gene pathways are in action to regulate ROS levels in RGPs during cortical development.…”

Section: Robust and Persistent Changes In Ros-related Gene Expressionmentioning

confidence: 99%

Oxidative stress regulates progenitor behavior and cortical neurogenesis

et al. 2020

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Orderly division of radial glial progenitors (RGPs) in the developing mammalian cerebral cortex generates deep and superficial layer neurons progressively. However, the mechanisms that control RGP behavior and precise neuronal output remain elusive. Here, we show that the oxidative stress level progressively increases in the developing mouse cortex and regulates RGP behavior and neurogenesis. As development proceeds, numerous gene pathways linked to reactive oxygen species (ROS) and oxidative stress exhibit drastic changes in RGPs. Selective removal of PRDM16, a transcriptional regulator highly expressed in RGPs, elevates ROS level and induces expression of oxidative stressresponsive genes. Coinciding with an enhanced level of oxidative stress, RGP behavior was altered, leading to abnormal deep and superficial layer neuron generation. Simultaneous expression of mitochondrially targeted catalase to reduce cellular ROS levels significantly suppresses cortical defects caused by PRDM16 removal. Together, these findings suggest that oxidative stress actively regulates RGP behavior to ensure proper neurogenesis in the mammalian cortex.

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“…Inflammation plays an important role in CRC [ 177 ] and it seems to be crucial in the toxin-induced pro-carcinogenic activity (see Figure 3 ). The establishment of chronic inflammation, in particular, can crucially contribute to cancer via different mechanisms, including the induction of the EMT, a process involved in metastasis, invasion, and progression of various cancers [ 178 , 179 ]. The ability to induce factors involved in EMT has first been reported for the protein toxins CagA and CagE, from the pro-carcinogenic bacteria H. pylori whose presence increases the proneness of patients to gastric cancer [ 180 , 181 , 182 ].…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?

Fiorentini¹,

Carlini

Germinario

et al. 2020

IJMS

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Accumulating evidence indicates that the human intestinal microbiota can contribute to the etiology of colorectal cancer. Triggering factors, including inflammation and bacterial infections, may favor the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. In this context, certain bacterial pathogens can exert a pro-tumoral activity by producing enzymatically-active protein toxins that either directly induce host cell DNA damage or interfere with essential host cell signaling pathways involved in cell proliferation, apoptosis, and inflammation. This review is focused on those toxins that, by mimicking carcinogens and cancer promoters, could represent a paradigm for bacterially induced carcinogenesis.

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Nitric oxide and interactions with reactive oxygen species in the development of melanoma, breast, and colon cancer: A redox signaling perspective

Cited by 66 publications

References 177 publications

Nitric oxide disrupts bacterial cytokinesis by poisoning purine metabolism

Nitric oxide disrupts bacterial cytokinesis by poisoning purine metabolism

Oxidative stress regulates progenitor behavior and cortical neurogenesis

Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?

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