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Cancer AND NOX

Meng-Shih Weng, Jer-Hwa Chang, Wen-Yueh Hung, Yi-Chieh Yang, Ming-Hsien Chien
BACKGROUND: The epidermal growth factor receptor (EGFR) plays important roles in cell survival, growth, differentiation, and tumorigenesis. Dysregulation of the EGFR is a common mechanism in cancer progression especially in non-small cell lung cancer (NSCLC). MAIN BODY: Suppression of the EGFR-mediated signaling pathway is used in cancer treatment. Furthermore, reactive oxygen species (ROS)-induced oxidative stress from mitochondrial dysfunction or NADPH oxidase (NOX) overactivation and ectopic expression of antioxidative enzymes were also indicated to be involved in EGFR-mediated tumor progression (proliferation, differentiation, migration, and invasion) and drug resistance (EGFR tyrosine kinase inhibitor (TKI))...
March 16, 2018: Journal of Experimental & Clinical Cancer Research: CR
Chao-Tao Tang, Xiao-Lu Lin, Shan Wu, Qian Liang, Li Yang, Yun-Jie Gao, Zhi-Zheng Ge
NADPH Oxidase 4 (NOX4), a member of the NOX family, has emerged as a significant source of reactive oxygen species, playing an important role in tumor cell proliferation, apoptosis, and other physiological processes. However, the potential function of NOX4 in gastric cancer (GC) cell proliferation is yet unknown. The aim of this study was to illustrate whether NOX4 plays a role in regulating gastric cancer cell growth. First, the clinical information from 90 patients was utilized to explore the clinical value of NOX4 as a predictive tool for tumor size and prognosis...
February 26, 2018: Cellular Signalling
Gali Cohen, Ilan Levy, Yuval, Jeremy D Kark, Noam Levin, Guy Witberg, Zaza Iakobishvili, Tamir Bental, David M Broday, David M Steinberg, Ran Kornowski, Yariv Gerber
Background Exposure to traffic-related air pollution (TRAP) is considered to have a carcinogenic effect. The authors previously reported a nonsignificant association between TRAP and cancer risk in a relatively small cohort of myocardial infarction survivors. This study assessed whether TRAP exposure is associated with subsequent cancer in a large cohort of coronary patients. Methods & results Consecutive patients undergoing percutaneous coronary interventions in a major medical centre in central Israel from 2004 to 2014 were followed for cancer through 2015...
January 1, 2018: European Journal of Preventive Cardiology
Xiaoting Jin, Ruijun Su, Ruijin Li, Long Cheng, Zhuoyu Li
Fine particulate matter exposure may cause health risk, including cardiovascular diseases and cancer. Bone marrow mesenchymal stem cell (BMSC), a typical model for evaluating pollutant toxicity, has been closely linked to these diseases, due to its characteristics of differentiation. We therefore studied the BMSCs differentiation and its roles in inflammatory activation in the respiratory tract upon PM2.5 exposure using both in vitro and in vivo models. BMSCs differentiation into endothelial-like cells (ELCs) and cancer-associated fibroblasts cells (CAFs) was enhanced in response to conditioned medium from PM2...
January 5, 2018: Oncotarget
Sandra J Page, Maria M Rivera, David E Kleiner, Xiongce Zhao, Sungyoung Auh, Elaine F Remmers, Theo Heller
Approximately 71 million people are chronically infected with the hepatitis C virus (HCV), a potentially lethal pathogen. HCV generates oxidative stress correlating with disease severity. HCV proteins increase reactive oxygen species production by stimulating nicotinamide adenine dinucleotide phosphate oxidase (NOX) activity. Reactive oxygen species are necessary for host defense and cell signaling; however, elevated NOX activity contributes to cancer, and NOX overexpression is associated with hepatic fibrosis...
November 2017: Hepatology Communications
Ji Hee Ha, Rangasudhagar Radhakrishnan, Muralidharan Jayaraman, Mingda Yan, Jeremy D Ward, Kar-Ming Fung, Katherine M Moxley, Anil K Sood, Ciro Isidoro, Priyabrata Mukherjee, Yong Sang Song, Danny N Dhanasekaran
Although hypoxia has been shown to reprogram cancer cells toward glycolytic shift, the identity of extrinsic stimuli that induce metabolic reprogramming independent of hypoxia, especially in ovarian cancer, is largely unknown. In this study, we use patient-derived ovarian cancer cells and high-grade serous ovarian cancer cell lines to demonstrate that lysophosphatidic acid (LPA), a lipid growth factor and GPCR ligand whose levels are substantially increased in ovarian cancer patients, triggers glycolytic shift in ovarian cancer cells...
January 31, 2018: Cancer Research
R Yahyapour, E Motevaseli, A Rezaeyan, H Abdollahi, B Farhood, M Cheki, S Rezapoor, D Shabeeb, A E Musa, M Najafi, V Villa
Every year, millions of cancer patients undergo radiation therapy for treating and destroying abnormal cell growths within normal cell environmental conditions. Thus, ionizing radiation can have positive therapeutic effects on cancer cells as well as post-detrimental effects on surrounding normal tissues. Previous studies in the past years have proposed that the reduction and oxidation metabolism in cells changes in response to ionizing radiation and has a key role in radiation toxicity to normal tissue. Free radicals generated from ionizing radiation result in upregulation of cyclooxygenases (COXs), nitric oxide synthase (NOSs), lipoxygenases (LOXs) as well as nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and their effected changes in mitochondrial functions are markedly noticeable...
January 9, 2018: Clinical & Translational Oncology
Weiqin Lu, Yumin Hu, Gang Chen, Zhao Chen, Hui Zhang, Feng Wang, Li Feng, Helene Pelicano, Hua Wang, Michael J Keating, Jinsong Liu, Wallace McKeehan, Huamin Wang, Yongde Luo, Peng Huang
[This corrects the article DOI: 10.1371/journal.pbio.1001326.].
December 2017: PLoS Biology
Li Jin, Zhe Hao Piao, Simei Sun, Bin Liu, Gwi Ran Kim, Young Mi Seok, Ming Quan Lin, Yuhee Ryu, Sin Young Choi, Hae Jin Kee, Myung Ho Jeong
Gallic acid (GA) has been reported to have beneficial effects on cancer, vascular calcification, and diabetes-induced myocardial dysfunction. We hypothesized that GA controls hypertension via oxidative stress response regulation in an animal model for essential hypertension. Spontaneously hypertensive rats (SHRs) were administered GA for 16 weeks. GA treatment lowered elevated systolic blood pressure in SHRs through the inhibition of vascular contractility and components of the renin-angiotensin II system. In addition, GA administration reduced aortic wall thickness and body weight in SHRs...
November 15, 2017: Scientific Reports
Xiang Gao, Jingping Sun, Chunyu Huang, Xiaohua Hu, Ning Jiang, Chenqi Lu
NADPH oxidase 4 (NOX4) is a member of the NADPH oxidase (NOX) family of enzymes and has been found abnormally expressed in human cancers. However, its role in gastric cancer (GC) is still unclear. In the current study, we reported that NOX4 expression levels were significantly up-regulated in GC tissues compared to normal tissues (P<0.0001). Higher NOX4 expression was significantly associated with poorer overall survival in GC patients. Silencing NOX4 in two NOX4 high expression GC cell lines, MGC-803 and BGC-823 cells, did not affect cell proliferation, while inhibited cell adhesion and cell invasion of GC cells...
2017: American Journal of Translational Research
Yasuyoshi Miyata, Tomohiro Matsuo, Yuji Sagara, Kojiro Ohba, Kaname Ohyama, Hideki Sakai
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...
October 22, 2017: International Journal of Molecular Sciences
Sinda Mahbouli, Audrey Der Vartanian, Sophie Ortega, Stéphanie Rougé, Marie-Paule Vasson, Adrien Rossary
NADPH oxidase (NOX) complexes (a family of seven isoforms) drive cellular ROS production in patho-logical processes such as cancer. NOX-driven ROS production is involved in cell mechanisms from signalling to oxidative stress. Leptin, an adipokine overexpressed in obese patients, has been investigated in studies on breast carcinogenesis, but its effects on oxidative stress remain largely unexplored, especially in breast cancer. The study used three human mammary epithelial cell models presenting different neoplastic status (healthy primary HMECs, neoplastic MCF-7 cells and neoplastic MDA-MB-231 cells) to determine the effects of leptin on short-term ROS production and to characterize the enzymes involved...
September 27, 2017: Oncology Reports
David Witte, Tobias Bartscht, Roland Kaufmann, Ralph Pries, Utz Settmacher, Hendrik Lehnert, Hendrik Ungefroren
Transforming growth factor (TGF)-β promotes epithelial-mesenchymal transition and cell invasion of cancer cells in part through the small GTPase RAC1. Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TGF-β1/RAC1-driven random cell migration (chemokinesis). Although the NOX isoforms NOX2, 4, 5, 6, and RAC1 were readily detectable by RT-PCR in pancreatic ductal adenocarcinoma (PDAC)-derived Panc1 and Colo357 cells, only NOX4 and RAC1 were expressed at higher levels comparable to those in peripheral blood monocytes...
October 12, 2017: Oncology Reports
Zorana J Andersen, Massimo Stafoggia, Gudrun Weinmayr, Marie Pedersen, Claudia Galassi, Jeanette T Jørgensen, Anna Oudin, Bertil Forsberg, David Olsson, Bente Oftedal, Gunn Marit Aasvang, Geir Aamodt, Andrei Pyko, Göran Pershagen, Michal Korek, Ulf De Faire, Nancy L Pedersen, Claes-Göran Östenson, Laura Fratiglioni, Kirsten T Eriksen, Anne Tjønneland, Petra H Peeters, Bas Bueno-de-Mesquita, Michelle Plusquin, Timothy J Key, Andrea Jaensch, Gabriele Nagel, Alois Lang, Meng Wang, Ming-Yi Tsai, Agnes Fournier, Marie-Christine Boutron-Ruault, Laura Baglietto, Sara Grioni, Alessandro Marcon, Vittorio Krogh, Fulvio Ricceri, Carlotta Sacerdote, Enrica Migliore, Ibon Tamayo-Uria, Pilar Amiano, Miren Dorronsoro, Roel Vermeulen, Ranjeet Sokhi, Menno Keuken, Kees de Hoogh, Rob Beelen, Paolo Vineis, Giulia Cesaroni, Bert Brunekreef, Gerard Hoek, Ole Raaschou-Nielsen
BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2...
October 13, 2017: Environmental Health Perspectives
Dirk Zboralski, Kai Hoehlig, Dirk Eulberg, Anna Frömming, Axel Vater
Immune checkpoint inhibitors promote T cell-mediated killing of cancer cells; however, only a subset of patients benefit from the treatment. A possible reason for this limitation may be that the tumor microenvironment (TME) is immune privileged, which may exclude cytotoxic T cells from the vicinity of cancer cells. The chemokine CXCL12 is key to the TME-driven immune suppression. In this study, we investigated the potential of CXCL12 inhibition by use of the clinical-stage l-RNA-aptamer NOX-A12 (olaptesed pegol) to increase the number of tumor-infiltrating lymphocytes...
September 28, 2017: Cancer Immunology Research
Hyuk Soo Eun, Sang Yeon Cho, Jong Seok Joo, Sun Hyung Kang, Hee Seok Moon, Eaum Seok Lee, Seok Hyun Kim, Byung Seok Lee
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex-derived reactive oxygen species (ROS) promote chronic liver inflammation and remodeling that can drive hepatocellular carcinoma development. The role of NOX expression in hepatocellular carcinoma (HCC) has been partially investigated; however, the clinical relevance of collective or individual NOX family member expression for HCC survival remains unclear. Here, we obtained NOX mRNA expression data for 377 HCC samples and 21 normal liver controls from the TCGA data portal and performed Kaplan-Meier survival, gene ontology functional enrichment, and gene set enrichment analyses...
September 11, 2017: Scientific Reports
Xīn Gào, Ben Schöttker
Oxidative stress results from an imbalance of the reactive oxygen species/reactive nitrogen species (ROS/RNS) production and the oxidants defense system. Extensive research during the last decades has revealed that oxidative stress can mediate cancer initiation and development by leading not only to molecular damage but also to a disruption of reduction-oxidation (redox) signaling. In order to provide a global overview of the redox signaling pathways, which play a role in cancer formation, we conducted a systematic literature search in PubMed and ISI Web of Science and identified 185 relevant reviews published in the last 10 years...
August 1, 2017: Oncotarget
Michelle Plusquin, Florence Guida, Silvia Polidoro, Roel Vermeulen, Ole Raaschou-Nielsen, Gianluca Campanella, Gerard Hoek, Soterios A Kyrtopoulos, Panagiotis Georgiadis, Alessio Naccarati, Carlotta Sacerdote, Vittorio Krogh, H Bas Bueno-de-Mesquita, W M Monique Verschuren, Sergi Sayols-Baixeras, Tommaso Panni, Annette Peters, Dennie G A J Hebels, Jos Kleinjans, Paolo Vineis, Marc Chadeau-Hyam
Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes...
August 23, 2017: Environment International
EunGi Kim, Wanyeon Kim, Sungmin Lee, Jahyun Chun, JiHoon Kang, Gaeul Park, IkJoon Han, Hee Jung Yang, HyeSook Youn, BuHyun Youn
Normal fibroblasts surrounding tumor cells play a crucial role in cancer progression through formation of the tumor microenvironment. Because factors secreted from normal fibroblasts can modulate the tumor microenvironment, it is necessary to identify key factors associated with regulation of secreted factors and to investigate the molecular mechanisms contributing to the tumor microenvironment formation process. In this study, we found that radiation induced the expression and K63-linkage poly-ubiquitination of TRAF4 in normal lung fibroblasts...
August 21, 2017: Scientific Reports
Dina Vara, Joanna M Watt, Tiago M Fortunato, Harry Mellor, Matthew Burgess, Kate Wicks, Kimberly Mace, Shaun Reeksting, Anneke Lubben, Caroline P D Wheeler-Jones, Giordano Pula
AIMS: Deoxyribose-1-phosphate (dRP) is a proangiogenic paracrine stimulus released by cancer cells, platelets, and macrophages and acting on endothelial cells. The objective of this study was to clarify how dRP stimulates angiogenic responses in human endothelial cells. RESULTS: Live cell imaging, electron paramagnetic resonance, pull-down of dRP-interacting proteins, followed by immunoblotting, gene silencing of different NADPH oxidases (NOXs), and their regulatory cosubunits by small interfering RNA (siRNA) transfection, and experiments with inhibitors of the sugar transporter glucose transporter 1 (GLUT1) were utilized to demonstrate that dRP acts intracellularly by directly activating the endothelial NOX2 complex, but not NOX4...
January 10, 2018: Antioxidants & Redox Signaling
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