Hydrogen peroxide – production, fate and role in redox signaling of tumor cells

Lennicke, Claudia; Rahn, Jette; Lichtenfels, Rudolf; Wessjohann, Ludger A.; Seliger, Barbara

doi:10.1186/s12964-015-0118-6

Cited by 459 publications

(367 citation statements)

References 244 publications

(211 reference statements)

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“…ROS or electrophilic agents modify redox-sensitive cysteine residues of Keap1, leading to conformational changes and the release of Nrf2, which in turn could translocate into the nucleus and initiate the transcriptional induction of its target proteins. 42 In our study, a strong upregulation of Nrf2 targets was observed, such as NQO1. Next to its role in the anti-oxidative defense, NQO1 is described to stabilize p53 and thus prevents its proteasomal degradation.…”

Section: Discussionsupporting

confidence: 59%

“…The expression pattern of three of the upregulated proteins are controlled by the transcription factor Nrf2. 42 These include glucose 6-phosphate dehydrogenase (G6PD), peroxiredoxin 1 (PRXD1) and S-formylglutathione hydrolase (ESTD), all involved in mounting/maintaining the anti-oxidative defense. In addition, two ER-resident enzymes named protein disulfide isomerase (PDI) and calreticulin (CALR) were upregulated in response to MSA treatment.…”

Section: Msa-mediated Changes In the Protein Expression Pattern Of B1mentioning

confidence: 99%

“…4B). Since PRDX1 and G6PDH are both regulated by Nrf2, 42 the expression level of the latter was determined by Western blot analysis. As shown in Fig.…”

Section: Validation Of Representative Differentially Expressed Proteimentioning

confidence: 99%

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Modulation of MHC class I surface expression in B16F10 melanoma cells by methylseleninic acid

et al. 2017

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The essential trace element selenium (Se) might play a role in cancer prevention as well as for cancer therapy. Its metabolite methylselenol is able to kill cells through distinct mechanisms including induction of reactive oxygen species, DNA damage and apoptosis. Since methylselenol affects innate immune responses by modulating the expression of NKG2D ligands, the aim of this study was to determine whether the methylselenol generating compound methylseleninic acid (MSA) influences the expression of the MHC class I surface antigens and growth properties thereby reverting immune escape.Treatment of B16F10 melanoma cells expressing low basal MHC class I surface antigens with dimethyldiselenide (DMDSe) and MSA, but not with selenomethionine and selenite resulted in a dosedependent upregulation of MHC class I cell surface antigens. This was due to a transcriptional upregulation of some major components of the antigen processing machinery (APM) and the interferon (IFN) signaling pathway and accompanied by a reduced migration of B16F10 melanoma cells in the presence of MSA. Comparative "ome"-based profilings of untreated and MSA-treated melanoma cells linked the anti-oxidative response system with MHC class I antigen processing. Since MSA treatment enhanced MHC class I surface expression also on different human tumors cell lines, MSA might affect the malignant phenotype of various tumor cells by restoring MHC class I APM component expression due to an altered redox status and by partially mimicking IFN-gamma signaling thereby providing a novel mechanism for the chemotherapeutic potential of methylselenol generating Se compounds.

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Section: Discussionsupporting

confidence: 59%

Section: Msa-mediated Changes In the Protein Expression Pattern Of B1mentioning

confidence: 99%

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Modulation of MHC class I surface expression in B16F10 melanoma cells by methylseleninic acid

et al. 2017

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“…In contrast to the superoxide anion and hydroxyl radical, the less reactive H 2 O 2 is involved in various signal transduction pathways in normal as well as in cancer cells, including proliferation and differentiation [189,190,reviewed in 191] as well as inflammation, phagocytosis and apoptosis [192]. The mechanism of "redox signaling" involves the H 2 O 2 -mediated reversible oxidation of specific amino acids in enzymes and transcription factors, thereby altering their activities [187,193].…”

Section: Hydrogen Peroxide As Signaling Moleculesmentioning

confidence: 99%

“…Increased ROS levels may play a significant role in cancer development by activating various signaling pathways [193,198]. Simply put, increased H 2 O 2 values may be perceived as "redox signaling".…”

Section: Hydrogen Peroxide As Signaling Moleculesmentioning

confidence: 99%

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

Köpp¹

2017

J Carcinog Mutagen

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In all western societies, mortality rates from cancer are high and even increasing. In striking contrast, cancer rates are very rare and even non-existent in primitive cultures, like hunter-gatherer (HG) populations. HGs are free of disease as long as they adhere to their traditional low-insulinemic "Paleolithic" nutrition. With acculturation and transition to current high-carbohydrate/high-insulinemic "Western" diets (HCHIDs), cancer develops in high rates. This paper follows the question of how significant nutritional changes, brought about by the Agricultural revolution, may cause development of cancer. The evidence presented shows that the switch from a Paleolithic to a Western nutrition has brought about significant metabolic perturbations, like an abnormally increased activation of the insulinlike growth factor system, the sympathetic nervous system and the renin-angiotensin-system, an increased expression of HIF-1α and other more, all of which are deeply involved in cancer development through promotion of proliferation, angiogenesis, inflammation, macrophage infiltration, metastasis and inhibition of apoptosis.In addition, HCHIDs generate oxidative stress which may cause mitochondrial damage and genomic instability, and may interfere with normal stem cell development. Faulty redox signaling is suggested to play a significant role in cancer development: hydrogen peroxide, generated at low concentrations, represents an important chemical mediator in the regulation of various cellular signal transduction processes, including stem cell development. Oxidative stress may be sensed by cells as redox signaling. Faulty "redox signaling" is proposed to affect normal stem cell development by sustained activation of uncoupling protein 2, leading to inhibition of differentiation ("maturation arrest"), sustained uncontrolled proliferation, and glycolysis with high expression of hexokinase II, typical features of cancer. In summary, an abnormal diet-related activation of various metabolic systems, together with faulty redox signaling, is suggested to play a pivotal role in cancer development.

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Ultrasound‐Activated Oxygen and ROS Generation Nanosystem Systematically Modulates Tumor Microenvironment and Sensitizes Sonodynamic Therapy for Hypoxic Solid Tumors

Zhu

et al. 2019

Adv Funct Materials

189

119

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Sonodynamic therapy (SDT) is noninvasive and possesses high bodypenetration depth, showing great potential for the treatment of deep-seated solid tumors. The efficacy of SDT, however, is limited by widespread hypoxia in solid tumors. Given this, an ultrasound-activated nanosystem is developed by integrating ferrate(VI) and protoporphyrin IX into biodegradable hollow mesoporous organosilica nanoplatforms, followed by assembling a phasechange material of lauric acid. The ferrate(VI) effectively reacts with water as well as overexpressed hydrogen peroxide and glutathione (GSH) in tumor cells, leading to tumor-microenvironment-independent oxygen production and in situ GSH depletion in tumors. More importantly, significant reactive oxygen species (ROS) overproduction is simultaneously achieved by protoporphyrin-augmented SDT and intracellular Fenton chemistry. Furthermore, the mild hyperthermia induced by ultrasound can trigger the phase change of lauric acid, achieving ultrasound-responsive control over the release of oxygen and ROS, and the depletion of GSH. The simultaneous oxygen generation, in situ GSH depletion, and ROS overproduction play a synergetic role in sensitizing SDT toward hypoxic solid tumors, which is verified by the remarkable improvement of hypoxic environments and more significant growth inhibition of SDT against osteosarcoma both in vitro and in vivo, showing promising application in hypoxic solid tumor treatment.

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Hydrogen peroxide – production, fate and role in redox signaling of tumor cells

Cited by 459 publications

References 244 publications

Modulation of MHC class I surface expression in B16F10 melanoma cells by methylseleninic acid

Modulation of MHC class I surface expression in B16F10 melanoma cells by methylseleninic acid

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

Ultrasound‐Activated Oxygen and ROS Generation Nanosystem Systematically Modulates Tumor Microenvironment and Sensitizes Sonodynamic Therapy for Hypoxic Solid Tumors

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