keyword
MENU ▼
Read by QxMD icon Read
search

Cancer AND NadPH

keyword
https://www.readbyqxmd.com/read/28626501/nadph-oxidases-insights-into-selected-functions-and-mechanisms-of-action-in-cancer-and-stem-cells
#1
REVIEW
Magdalena Skonieczna, Tomasz Hejmo, Aleksandra Poterala-Hejmo, Artur Cieslar-Pobuda, Rafal J Buldak
NADPH oxidases (NOX) are reactive oxygen species- (ROS-) generating enzymes regulating numerous redox-dependent signaling pathways. NOX are important regulators of cell differentiation, growth, and proliferation and of mechanisms, important for a wide range of processes from embryonic development, through tissue regeneration to the development and spread of cancer. In this review, we discuss the roles of NOX and NOX-derived ROS in the functioning of stem cells and cancer stem cells and in selected aspects of cancer cell physiology...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28620580/the-human-nadph-oxidase-nox4-regulates-cytoskeletal-organization-in-two-cancer-cell-lines-hepg2-and-sh-sy5y
#2
Simon Auer, Mark Rinnerthaler, Johannes Bischof, Maria Karolin Streubel, Hannelore Breitenbach-Koller, Roland Geisberger, Elmar Aigner, Janne Cadamuro, Klaus Richter, Mentor Sopjani, Elisabeth Haschke-Becher, Thomas Klaus Felder, Michael Breitenbach
NADPH oxidases of human cells are not only functional in defense against invading microorganisms and for oxidative reactions needed for specialized biosynthetic pathways but also during the past few years have been established as signaling modules. It has been shown that human Nox4 is expressed in most somatic cell types and produces hydrogen peroxide, which signals to remodel the actin cytoskeleton. This correlates well with the function of Yno1, the only NADPH oxidase of yeast cells. Using two established tumor cell lines, which are derived from hepatic and neuroblastoma tumors, respectively, we are showing here that in both tumor models Nox4 is expressed in the ER (like the yeast NADPH oxidase), where according to published literature, it produces hydrogen peroxide...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28607489/the-metabolic-function-of-cyclin-d3-cdk6-kinase-in-cancer-cell-survival
#3
Haizhen Wang, Brandon N Nicolay, Joel M Chick, Xueliang Gao, Yan Geng, Hong Ren, Hui Gao, Guizhi Yang, Juliet A Williams, Jan M Suski, Mark A Keibler, Ewa Sicinska, Ulrike Gerdemann, W Nicholas Haining, Thomas M Roberts, Kornelia Polyak, Steven P Gygi, Nicholas J Dyson, Piotr Sicinski
D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3-CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2...
June 15, 2017: Nature
https://www.readbyqxmd.com/read/28584401/chemopreventive-effects-of-a-low-side-effect-antibiotic-drug-erythromycin-on-mouse-intestinal-tumors
#4
Takahiro Hamoya, Shingo Miyamoto, Susumu Tomono, Gen Fujii, Ruri Nakanishi, Masami Komiya, Shuya Tamura, Kyoko Fujimoto, Jiro Toshima, Keiji Wakabayashi, Michihiro Mutoh
It is important to establish effective methods for preventing colorectal cancer because the number of colorectal cancer deaths is increasing. Erythromycin one of the macrolide antibiotics, has been shown to exert pleiotropic effects, such as anti-inflammatory and anti-oxidative effects, on mammalian cells. In the present study, we aimed to evaluate the preventive effects of erythromycin on intestinal carcinogenesis. We first confirmed that erythromycin suppresses the transcriptional activity of nuclear factor-κB and activator protein-1 and the expression of its downstream targets, interleukin-6 and cyclooxygenase-2 in human colon cancer cells...
May 2017: Journal of Clinical Biochemistry and Nutrition
https://www.readbyqxmd.com/read/28578276/decoding-nadph-oxidase-4-expression-in-human-tumors
#5
Jennifer L Meitzler, Hala R Makhlouf, Smitha Antony, Yongzhong Wu, Donna Butcher, Guojian Jiang, Agnes Juhasz, Jiamo Lu, Iris Dahan, Pidder Jansen-Dürr, Haymo Pircher, Ajay M Shah, Krishnendu Roy, James H Doroshow
NADPH oxidase 4 (NOX4) is a redox active, membrane-associated protein that contributes to genomic instability, redox signaling, and radiation sensitivity in human cancers based on its capacity to generate H2O2 constitutively. Most studies of NOX4 in malignancy have focused on the evaluation of a small number of tumor cell lines and not on human tumor specimens themselves; furthermore, these studies have often employed immunological tools that have not been well characterized. To determine the prevalence of NOX4 expression across a broad range of solid tumors, we developed a novel monoclonal antibody that recognizes a specific extracellular region of the human NOX4 protein, and that does not cross-react with any of the other six members of the NOX gene family...
May 26, 2017: Redox Biology
https://www.readbyqxmd.com/read/28578013/paradoxical-roles-of-dual-oxidases-in-cancer-biology
#6
REVIEW
Andrew C Little, Arvis Sulovari, Karamatullah Danyal, David E Heppner, David J Seward, Albert van der Vliet
Dysregulated oxidative metabolism is a well-recognized aspect of cancer biology, and many therapeutic strategies are based on targeting cancers by altering cellular redox pathways. The NADPH oxidases (NOXes) present an important enzymatic source of biological oxidants, and the expression and activation of several NOX isoforms are frequently dysregulated in many cancers. Cell-based studies have demonstrated a role for several NOX isozymes in controlling cell proliferation and/or cell migration, further supporting a potential contributing role for NOX in promoting cancer...
May 31, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28574838/histone-modifications-affect-differential-regulation-of-tgf%C3%AE-induced-nadph-oxidase-4-nox4-by-wild-type-and-mutant-p53
#7
Howard E Boudreau, Wei Feng Ma, Agnieszka Korzeniowska, Jonathan J Park, Medha A Bhagwat, Thomas L Leto
Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFβ-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Here, we extended our findings on the effects of p53 on NOX4 in several tumors and examined the basis of NOX4 transcriptional regulation by p53 and SMAD3. Statistical analysis of expression data from primary tumors available from The Cancer Genome Atlas (TCGA) detected correlations between mut-p53 and increased NOX4 expression...
May 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28574504/nox2-dependent-atm-kinase-activation-dictates-pro-inflammatory-macrophage-phenotype-and-improves-effectiveness-to-radiation-therapy
#8
Qiuji Wu, Awatef Allouch, Audrey Paoletti, Celine Leteur, Celine Mirjolet, Isabelle Martins, Laurent Voisin, Frédéric Law, Haithem Dakhli, Elodie Mintet, Maxime Thoreau, Zeinaf Muradova, Mélanie Gauthier, Olivier Caron, Fabien Milliat, David M Ojcius, Filippo Rosselli, Eric Solary, Nazanine Modjtahedi, Eric Deutsch, Jean-Luc Perfettini
Although tumor-associated macrophages have been extensively studied in the control of response to radiotherapy, the molecular mechanisms involved in the ionizing radiation-mediated activation of macrophages remain elusive. Here we show that ionizing radiation induces the expression of interferon regulatory factor 5 (IRF5) promoting thus macrophage activation toward a pro-inflammatory phenotype. We reveal that the activation of the ataxia telangiectasia mutated (ATM) kinase is required for ionizing radiation-elicited macrophage activation, but also for macrophage reprogramming after treatments with γ-interferon, lipopolysaccharide or chemotherapeutic agent (such as cisplatin), underscoring the fact that the kinase ATM plays a central role during macrophage phenotypic switching toward a pro-inflammatory phenotype through the regulation of mRNA level and post-translational modifications of IRF5...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28564604/cancer-associated-idh1-promotes-growth-and-resistance-to-targeted-therapies-in-the-absence-of-mutation
#9
Andrea E Calvert, Alexandra Chalastanis, Yongfei Wu, Lisa A Hurley, Fotini M Kouri, Yingtao Bi, Maureen Kachman, Jasmine L May, Elizabeth Bartom, Youjia Hua, Rama K Mishra, Gary E Schiltz, Oleksii Dubrovskyi, Andrew P Mazar, Marcus E Peter, Hongwu Zheng, C David James, Charles F Burant, Navdeep S Chandel, Ramana V Davuluri, Craig Horbinski, Alexander H Stegh
Oncogenic mutations in two isocitrate dehydrogenase (IDH)-encoding genes (IDH1 and IDH2) have been identified in acute myelogenous leukemia, low-grade glioma, and secondary glioblastoma (GBM). Our in silico and wet-bench analyses indicate that non-mutated IDH1 mRNA and protein are commonly overexpressed in primary GBMs. We show that genetic and pharmacologic inactivation of IDH1 decreases GBM cell growth, promotes a more differentiated tumor cell state, increases apoptosis in response to targeted therapies, and prolongs the survival of animal subjects bearing patient-derived xenografts (PDXs)...
May 30, 2017: Cell Reports
https://www.readbyqxmd.com/read/28554049/increased-susceptibility-of-idh2-deficient-mice-to-dextran-sodium-sulfate-induced-colitis
#10
Hanvit Cha, Seoyoon Lee, Sung Hwan Kim, Hyunjin Kim, Dong-Seok Lee, Hyun-Shik Lee, Jin Hyup Lee, Jeen-Woo Park
Inflammatory bowel disease (IBD) is a group of chronic, relapsing, immunological, inflammatory disorders of the gastrointestinal tract including ulcerative colitis (UC) and Crohn's disease (CD). It has been reported that UC, which is studied using a dextran sodium sulfate (DSS)-induced colitis model, is associated with the production of reactive oxygen species (ROS) and the apoptosis of intestine epithelial cells (IEC). Mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDH2) has been reported as an essential enzyme in the mitochondrial antioxidant system via generation of NADPH...
May 20, 2017: Redox Biology
https://www.readbyqxmd.com/read/28542136/pak4-regulates-g6pd-activity-by-p53-degradation-involving-colon-cancer-cell-growth
#11
Xiumei Zhang, Xia Zhang, Yang Li, Yangguang Shao, Jianying Xiao, Ge Zhu, Feng Li
The p21-activated kinase 4 (PAK4) is overexpressed in different cancers and promotes proliferation of cancer cells. Reprogramming of glucose metabolism is found in most cancer cells which in turn supports rapid proliferation. However, the relationship between PAK4 and glucose metabolism in cancer cells has not been explored. In this study, we reported that PAK4 promoted glucose intake, NADPH production and lipid biosynthesis, leading to an increased proliferation of colon cancer cells. Mechanistically, PAK4 interacted with glucose-6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme of the pentose phosphate pathway and increased G6PD activity via enhancing Mdm2-mediated p53 ubiquitination degradation...
May 25, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28536313/dual-inhibition-of-nox2-and-receptor-tyrosine-kinase-by-bj-1301-enhances-anticancer-therapy-efficacy-via-suppression-of-autocrine-stimulatory-factors-in-lung-cancer
#12
Jaya Gautam, Jin-Mo Ku, Sushil Chandra Regmi, Hyunyoung Jeong, Ying Wang, Suhrid Banskota, Myo-Hyeon Park, Tae-Gyu Nam, Byeong-Seon Jeong, Jung-Ae Kim
NADPH oxidase-derived reactive oxygen species (ROS) potentiate receptor tyrosine kinase (RTK) signalling, resulting in enhanced angiogenesis and tumor growth. In the present study, we report that BJ-1301, a hybrid of pyridinol and alpha-tocopherol, exerts anticancer effects by dual inhibition of NADPH oxidase and RTK activities in endothelial and lung cancer cells. BJ-1301 suppresses ROS production by blocking translocation of NADPH oxidase cytosolic subunits to the cell membrane, thereby inhibiting activation...
May 23, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28518138/betulin-exhibits-anti-inflammatory-activity-in-lps-stimulated-macrophages-and-endotoxin-shocked-mice-through-an-ampk-akt-nrf2-dependent-mechanism
#13
Xinxin Ci, Junfeng Zhou, Hongming Lv, Qinlei Yu, Liping Peng, Shucheng Hua
Continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer. Nuclear factor erythroid 2-related factor (Nrf2), a critical transcriptional activator for antioxidative responses, has envolved to be an attractive drug target for the treatment or prevention of human diseases. In the present study, we investigated the effects and mechanisms of betulin on Nrf2 activation and its involvement in the lipopolysaccharide (LPS)-triggered inflammatory system...
May 18, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28510506/signaling-at-the-crossroads-matrix-derived-proteoglycan-and-reactive-oxygen-species-signaling
#14
Madalina-Viviana Nastase, Andrea Janicova, Malgorzata Wygrecka, Liliana Schaefer
SIGNIFICANCE: Proteoglycans (PGs), besides their structural contribution, have emerged as dynamic components that mediate a multitude of cellular events. The various roles of PGs are attributed to their structure, spatial localization, and ability to act as ligands and receptors. Reactive oxygen species (ROS) are small mediators, which are generated in physiological and pathological conditions. Besides their reactivity and ability to induce oxidative stress, a growing body of data suggests that ROS signaling is more relevant than direct radical damage in development of human pathologies...
May 16, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28498822/interleukin-4-and-interleukin-13-increase-nadph-oxidase-1-related-proliferation-of-human-colon-cancer-cells
#15
Han Liu, Smitha Antony, Krishnendu Roy, Agnes Juhasz, Yongzhong Wu, Jiamo Lu, Jennifer L Meitzler, Guojian Jiang, Eric Polley, James H Doroshow
Human colon cancers express higher levels of NADPH oxidase 1 [NOX1] than adjacent normal epithelium. It has been suggested that reactive oxygen species [ROS] derived from NOX1 contribute to DNA damage and neoplastic transformation in the colon, particularly during chronic inflammatory stress. However, the mechanism(s) underlying increased NOX1 expression in malignant tumors or chronic inflammatory states involving the intestine are poorly characterized. We examined the effects of two pro-inflammatory cytokines, IL-4 and IL-13, on the regulation of NOX1...
June 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28482870/effect-of-the-cancer-specific-shorter-form-of-human-6-phosphofructo-1-kinase-on-the-metabolism-of-the-yeast-saccharomyces-cerevisiae
#16
Darjan Andrejc, Alenka Možir, Matic Legiša
BACKGROUND: At first glance, there appears to be a high degree of similarity between the metabolism of yeast (the Crabtree effect) and human cancer cells (the Warburg effect). At the root of both effects is accelerated metabolic flow through glycolysis which leads to overflows of ethanol and lactic acid, respectively. It has been proposed that enhanced glycolytic flow in cancer cells is triggered by the altered kinetic characteristics of the key glycolytic regulatory enzyme 6-phosphofructo-1-kinase (Pfk)...
May 8, 2017: BMC Biotechnology
https://www.readbyqxmd.com/read/28481367/inhibition-of-malic-enzyme-1-disrupts-cellular-metabolism-and-leads-to-vulnerability-in-cancer-cells-in-glucose-restricted-conditions
#17
S Murai, A Ando, S Ebara, M Hirayama, Y Satomi, T Hara
Malic enzyme 1 (ME1) regulates one of the main pathways that provide nicotinamide adenine dinucleotide phosphate (NADPH), which is essential for cancer cell growth through maintenance of redox balance and biosynthesis processes in the cytoplasm. In this study, we found that ME1 inhibition disrupted metabolism in cancer cells and inhibited cancer cell growth by inducing senescence or apoptosis. In glucose-restricted culture conditions, cancer cells increased ME1 expression, and tracer experiments with labelled glutamine revealed that the flux of ME1-derived pyruvate to citrate was enhanced...
May 8, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28476935/a-schistosoma-japonicum-infection-promotes-the-expansion-of-myeloid-derived-suppressor-cells-by-activating-the-jak-stat3-pathway
#18
Quan Yang, Huaina Qiu, Hongyan Xie, Yanwei Qi, Hefei Cha, Jiale Qu, Mei Wang, Yuanfa Feng, Xin Ye, Jianbing Mu, Jun Huang
Myeloid-derived suppressor cells (MDSCs), a heterogeneous group of immune cells from the myeloid lineage, play an important part in suppression of host immune responses during many pathologic conditions, including cancer and infectious diseases. Thus, understanding the functional diversity of these cells as well as the underlying mechanisms is crucial for the development of disease control strategies. The role of MDSCs during Schistosoma japonicum infection, however, is not clear, and there is a lack of systematic study so far...
June 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28475173/microrna-30a-attenuates-mutant-kras-driven-colorectal-tumorigenesis-via-direct-suppression-of-me1
#19
Hongxing Shen, Chuan Xing, Kaisa Cui, Yunxiao Li, Jinxiang Zhang, Runlei Du, Xiaodong Zhang, Youjun Li
Frequent KRAS mutations contribute to multiple cancers including ~40% of human colorectal cancers (CRCs). Systematic screening of 1255 microRNAs (miRNAs) identified miR-30a as a synthetic lethal in KRAS-mutant CRC cells. miR-30a was downregulated in CRCs and repressed by P65. miR-30a directly targeted malic enzyme 1 (ME1) and KRAS, and inhibited anchorage-independent growth and in vivo tumorigenesis by KRAS-mutant CRC cells. ME1 was significantly upregulated in KRAS-mutant CRCs. Eliminating ME1 by short hairpin RNA (shRNA) resulted in obviously decreased NADPH production, levels of triglyceride and fatty acid, and an inhibition of tumorigenicity of KRAS-mutant CRCs...
May 5, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28473742/nadph-oxidase-activation-contributes-to-heavy-ion-irradiation-induced-cell-death
#20
Yupei Wang, Qing Liu, Weiping Zhao, Xin Zhou, Guoying Miao, Chao Sun, Hong Zhang
Increased oxidative stress plays an important role in heavy ion radiation-induced cell death. The mechanism involved in the generation of elevated reactive oxygen species (ROS) is not fully illustrated. Here we show that NADPH oxidase activation is closely related to heavy ion radiation-induced cell death via excessive ROS generation. Cell death and cellular ROS can be greatly reduced in irradiated cancer cells with the preincubation of diphenyleneiodium, an inhibitor of NADPH oxidase. Most of the NADPH oxidase (NOX) family proteins (NOX1, NOX2, NOX3, NOX4, and NOX5) showed increased expression after heavy ion irradiation...
January 2017: Dose-response: a Publication of International Hormesis Society
keyword
keyword
108645
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"