Targeting Nrf2 in healthy and malignant ovarian epithelial cells: Protection versus promotion

Wijst, Monique G. P. van der; Huisman, Christian; Mposhi, Archibold; Roelfes, Gérard; Rots, Marianne G.

doi:10.1016/j.molonc.2015.03.003

Cited by 16 publications

(16 citation statements)

References 66 publications

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“…As previously described 59 , sensitivity toward ROS-induced cell death was determined using propidium iodide (PI) as marker for late apoptotic/necrotic cells. Cells were stained for 10 min with 5 μg/mL PI (Sigma-Aldrich) in PBS at 4 °C in the dark.…”

Section: Methodsmentioning

confidence: 99%

Experimental mitochondria-targeted DNA methylation identifies GpC methylation, not CpG methylation, as potential regulator of mitochondrial gene expression

Wijst

Tilburg

Ruiters

et al. 2017

Sci Rep

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Like the nucleus, mitochondria contain their own DNA and recent reports provide accumulating evidence that also the mitochondrial DNA (mtDNA) is subjective to DNA methylation. This evidence includes the demonstration of mitochondria-localised DNA methyltransferases and demethylases, and the detection of mtDNA methylation as well as hydroxymethylation. Importantly, differential mtDNA methylation has been linked to aging and diseases, including cancer and diabetes. However, functionality of mtDNA methylation has not been demonstrated. Therefore, we targeted DNA methylating enzymes (modifying cytosine in the CpG or GpC context) to the mtDNA. Unexpectedly, mtDNA gene expression remained unchanged upon induction of CpG mtDNA methylation, whereas induction of C-methylation in the GpC context decreased mtDNA gene expression. Intriguingly, in the latter case, the three mtDNA promoters were differentially affected in each cell line, while cellular function seemed undisturbed. In conclusion, this is the first study which directly addresses the potential functionality of mtDNA methylation. Giving the important role of mitochondria in health and disease, unravelling the impact of mtDNA methylation adds to our understanding of the role of mitochondria in physiological and pathophysiological processes.

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Section: Methodsmentioning

confidence: 99%

Experimental mitochondria-targeted DNA methylation identifies GpC methylation, not CpG methylation, as potential regulator of mitochondrial gene expression

Wijst

Tilburg

Ruiters

et al. 2017

Sci Rep

Self Cite

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“…KEAP1 fosters IKKβ ubiquitination and autophagic degradation, thus allowing the downregulation of NF-κΒ signaling 53,71 . Accordingly, with the cytoprotective role of Nrf2 in tumor cells 72,73 , Lee and colleagues demonstrated that proteasome inhibitors favored IκBα degradation by triggering Nrf2-mediated autophagy.…”

Section: Nf-κb Regulates Autophagy In Cancer Cellsmentioning

confidence: 99%

Life, death, and autophagy in cancer: NF-κB turns up everywhere

et al. 2020

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Escaping programmed cell death is a hallmark of cancer. NF-κB transcription factors are key regulator of cell survival and aberrant NF-κB signaling has been involved in the pathogenesis of most human malignancies. Although NF-κB is best known for its antiapoptotic role, other processes regulating the life/death balance, such as autophagy and necroptosis, seem to network with NF-κB. This review discusses how the reciprocal regulation of NF-κB, autophagy and programmed cell death affect cancer development and progression.

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“…Thioredoxin is involved in redox regulation of transcription factors such as NF-κB, NRF2, forkhead box class O (FOXO) proteins, reducing factor-1 (ref-1), and hypoxia inducible factor (HIF-1α), thereby increasing their binding to the DNA. Most of these transcription factors promote tumor growth and progression by regulating expression of genes that affect cell survival and growth [ 83 , 84 ]. For example, FOXO, NRF2, and ref-1 transcription factors upregulate transcription of anti-oxidant proteins that scavenge free radicals and allow survival of damaged or transformed cells [ 85 ].…”

Section: Inflammation and Eoc Initiation And Progressionmentioning

confidence: 99%

The Role of Inflammation and Inflammatory Mediators in the Development, Progression, Metastasis, and Chemoresistance of Epithelial Ovarian Cancer

Savant

Sriramkumar

O’Hagan

2018

Cancers

133

111

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Inflammation plays a role in the initiation and development of many types of cancers, including epithelial ovarian cancer (EOC) and high grade serous ovarian cancer (HGSC), a type of EOC. There are connections between EOC and both peritoneal and ovulation-induced inflammation. Additionally, EOCs have an inflammatory component that contributes to their progression. At sites of inflammation, epithelial cells are exposed to increased levels of inflammatory mediators such as reactive oxygen species, cytokines, prostaglandins, and growth factors that contribute to increased cell division, and genetic and epigenetic changes. These exposure-induced changes promote excessive cell proliferation, increased survival, malignant transformation, and cancer development. Furthermore, the pro-inflammatory tumor microenvironment environment (TME) contributes to EOC metastasis and chemoresistance. In this review we will discuss the roles inflammation and inflammatory mediators play in the development, progression, metastasis, and chemoresistance of EOC.

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Targeting Nrf2 in healthy and malignant ovarian epithelial cells: Protection versus promotion

Cited by 16 publications

References 66 publications

Experimental mitochondria-targeted DNA methylation identifies GpC methylation, not CpG methylation, as potential regulator of mitochondrial gene expression

Experimental mitochondria-targeted DNA methylation identifies GpC methylation, not CpG methylation, as potential regulator of mitochondrial gene expression

Life, death, and autophagy in cancer: NF-κB turns up everywhere

The Role of Inflammation and Inflammatory Mediators in the Development, Progression, Metastasis, and Chemoresistance of Epithelial Ovarian Cancer

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