scholarly journals Role of Pirin, an Oxidative Stress Sensor Protein, in Epithelial Carcinogenesis

2020 ◽  
Author(s):  
Francisco Perez-Dominguez ◽  
Diego Carrillo-Beltrán ◽  
Rancés Blanco ◽  
Juan P. Muñoz ◽  
Grettell León-Cruz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Development ◽  
Biological Factors ◽  
Epithelial Cancers ◽  
Physical Chemical ◽  
Sensor Protein ◽  
Cupin Superfamily ◽  
Functionally Diverse ◽  
Light Chain Enhancer

Pirin is an oxidative stress (OS) sensor belonging to the functionally diverse cupin superfamily of proteins. Pirin is a suggested quercetinase and transcriptional activator of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Its biological role in cancer development remains as a novel area of study. This review shows accumulating evidence on the contribution of Pirin in epithelial cancers, signaling pathways involved, and as a suggested therapeutic target. Finally, we propose a model in which Pirin is upregulated by physical, chemical or biological factors involved in OS and cancer development.

scholarly journals Role of Pirin, an Oxidative Stress Sensor Protein, in Epithelial Carcinogenesis

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 116
Author(s):  
Francisco Perez-Dominguez ◽  
Diego Carrillo-Beltrán ◽  
Rancés Blanco ◽  
Juan P. Muñoz ◽  
Grettell León-Cruz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Development ◽  
Biological Factors ◽  
Epithelial Cancers ◽  
Physical Chemical ◽  
Sensor Protein ◽  
Cupin Superfamily ◽  
Functionally Diverse ◽  
Light Chain Enhancer

Pirin is an oxidative stress (OS) sensor belonging to the functionally diverse cupin superfamily of proteins. Pirin is a suggested quercetinase and transcriptional activator of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Its biological role in cancer development remains a novel area of study. This review presents accumulating evidence on the contribution of Pirin in epithelial cancers, involved signaling pathways, and as a suggested therapeutic target. Finally, we propose a model in which Pirin is upregulated by physical, chemical or biological factors involved in OS and cancer development.

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

Toxins ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 199 ◽  
Author(s):  
Karolina Kowalska ◽  
Dominika Ewa Habrowska-Górczyńska ◽  
Kamila Domińska ◽  
Kinga Anna Urbanek ◽  
Agnieszka Wanda Piastowska-Ciesielska
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
M Cell ◽  
Androgen Independence ◽  
Prostate Carcinogenesis ◽  
Cycle Arrest ◽  
Light Chain Enhancer

Nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) is commonly expressed in prostate cancer (PCa) cells and is associated with increased proliferation, metastases and androgen independence. Zearalenone (ZEA) is one of the most common mycotoxins contaminating food, which might mimic estrogens and bind to estrogen receptors (ERs). The ratio of androgens to estrogens in men decreases physiologically with age, and is believed to participate in prostate carcinogenesis. In this study, we evaluated the role of NFκB and ERβ in the induction of oxidative stress in human PCa cells by ZEA. As observed, ZEA at a dose of 30 µM induces oxidative stress in PCa cells associated with DNA damage and G2/M cell cycle arrest. We also observed that the inhibition of ERβ and NFΚB via specific inhibitors (PHTPP and BAY 117082) significantly increased ZEA-induced oxidative stress, although the mechanism seems to be different for androgen-dependent and androgen-independent cells. Based on our findings, it is possible that the activation of ERβ and NFΚB in PCa might protect cancer cells from ZEA-induced oxidative stress. We therefore shed new light on the mechanism of ZEA toxicity in human cells.

scholarly journals The role of heme oxygenase in metastatic melanoma tumorigenicity

2015 ◽  
Author(s):  
◽  
Kimberly J. Jasmer
Keyword(s):  
Oxidative Stress ◽  
Metastatic Melanoma ◽  
Heme Oxygenase ◽  
Focal Adhesion ◽  
Target Genes ◽  
Cancer Development ◽  
Heme Oxygenase Activity ◽  
Oxygenase Activity ◽  
Receptor Interactions

Reactive oxygen species (ROS) are highly reactive, tumorigenic molecules. In response to ROS accumulation, or oxidative stress, the transcription factor Nrf2 promotes expression by binding antioxidant response elements (AREs) found in the promoter of target genes. Traditionally, Nrf2 has been considered inhibitory of cancer by promoting the expression of phase II detoxifying enzymes, drug transporters, anti-apoptotic proteins, and proteasomes, which facilitate the removal of ROS and promote cell survival. Recently, however, overexpression of Nrf2-target genes has been implicated in promoting several cancer hallmarks and facilitating cancer development. Significant focus has been given to the role of Keap1/Nrf2 as a sensor for oxidative stress. Much less attention has been paid to the role of Bach1, a transcriptional repressor that competes with Nrf2 for ARE binding. The best-characterized Bach1 target is Heme Oxygenase-1 (HMOX1). While heme oxygenase inhibits cancer by preventing ROS-induced damage, mounting evidence suggests that HMOX1 overexpression at later stages in cancer development may promote cancer progression. Heme oxygenase catalyzes the degradation of heme and has two isozymes. HMOX1 is inducible by heme and oxidative stress while HMOX2 is constitutively expressed. Stage IV metastatic melanoma has a median survival of only 6 to 10 months. Unfortunately, current therapeutic approaches provide limited benefit in overall survival, highlighting the need for the identification of novel therapeutic targets. Activating mutations in B-Raf are found in approximately 70% of malignant melanomas. Using an anchorage-independent melanosphere assay, which is indicative of the tumorigenicity of melanoma cells, we found that activation of B-Raf, but not N-Ras, is a driver of melanosphere formation. We provide evidence that derepression of Bach1 by treatment with cobalt protoporphyrin IX (CoPP) is sufficient for melanosphere formation, and that melanosphere formation induced by either CoPP treatment or B-Raf activation is dependent on heme oxygenase activity. Global transcriptome analysis revealed enrichment for genes involved in focal adhesion and extracellular matrix (ECM)-receptor interactions following either B-Raf activation or treatment with CoPP. We propose a mechanism by which heme oxygenase promotes melanosphere formation, and by extension, enhanced tumorigenicity, by modulating expression of genes involved in focal adhesion and ECM-receptor interactions. Heme oxygenase activity may provide a novel therapeutic target for the treatment of metastatic melanoma.

scholarly journals The influence of inflammaging on oncogenesis

2019 ◽  
Vol 75 (01) ◽  
pp. 6164-2019
Author(s):  
JANUSZ A. MADEJ
Keyword(s):  
Oxidative Stress ◽  
Point Mutations ◽  
Endocrine System ◽  
Gonadotropin Releasing Hormone ◽  
Surrounding Tissue ◽  
Nuclear Factor ◽  
Kappa Light Chain ◽  
Dependent Processes ◽  
Light Chain Enhancer

There is a specific antagonism between an aging organism and neoplasia, in which the tumor is considered to influence the local tissue. It returns to some atavistic features, including the thermodynamic approach (2nd law of thermodynamics, Fig. 1), causing the rejuvenation of the surrounding tissue. The existence of various theories of oncogenesis entitles their supplementation with the theory of inflammaging: an entropic inflammation that can potentially have an indirect influence on the oncogenesis. This theory covers the effects of various causes of aging, including genetically programmed changes, telomere dependent processes and damage of genome, epigenome and proteome particles. The paper describes the patomechanism of inflammaging, including the role of mitochondria (point mutations and deletions especially in mtDNA), oxidative stress with overproduction and accumulation of free radicals and NFkB factor (nuclear factor kappa-light chain-enhancer of activated B cells) and the possibility of the influence of inflammaging on oncogenesis (Fig. 2). The inflamma-ging is programmed by hypothalamus using the immune-neuro-endocrine system, including gonadotropin releasing hormone (GnRH) that inhibits the NFkB factor with the inactivation of kinase IKK-beta. Regardless of that, the chronic inflammation, exceeding its defensive competence, lasts for years and can also be the beginning of neoplastic cells proliferation.

The role of oxidative stress on breast cancer development and therapy

Tumor Biology ◽  
2016 ◽  
Vol 37 (4) ◽  
pp. 4281-4291 ◽  
Author(s):  
Fabio Hecht ◽  
Carolina F. Pessoa ◽  
Luciana B. Gentile ◽  
Doris Rosenthal ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Development ◽  
Breast Cancer Development

Elevated mercury concentrations in fish in lakes in the Mackenzie River Basin: The role of physical, chemical, and biological factors

2005 ◽  
Vol 351-352 ◽  
pp. 479-500 ◽  
Author(s):  
M.S. Evans ◽  
W.L. Lockhart ◽  
L. Doetzel ◽  
G. Low ◽  
D. Muir ◽  
...  
Keyword(s):  
River Basin ◽  
Biological Factors ◽  
Physical Chemical ◽  
Mackenzie River Basin ◽  
Mackenzie River

scholarly journals Role of Oxidative Stress and the Microenvironment in Breast Cancer Development and Progression

2013 ◽  
pp. 107-125 ◽  
Author(s):  
Agnieszka Jezierska-Drutel ◽  
Steven A. Rosenzweig ◽  
Carola A. Neumann
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Development ◽  
Breast Cancer Development

792: Role of Oxidative Stress in Tumorigenic Potential of Bladder Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 214-215 ◽  
Author(s):  
Daniel Cho ◽  
Xiao Fang Ha ◽  
J. Andre Melendez ◽  
Louis J. Giorgi ◽  
Badar M. Mian
Keyword(s):  
Oxidative Stress ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Tumorigenic Potential ◽  
Bladder Cancer Cells
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