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Cancer AND NadPH

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https://www.readbyqxmd.com/read/29445082/pyruvate-kinase-m2-regulates-photoreceptor-structure-function-and-viability
#1
Ammaji Rajala, Yuhong Wang, Richard S Brush, Kristine Tsantilas, Connor S R Jankowski, Ken J Lindsay, Jonathan D Linton, James B Hurley, Robert E Anderson, Raju V S Rajala
Pyruvate kinase M2 (PKM2) is a glycolytic enzyme that is expressed in cancer cells. Its role in tumor metabolism is not definitively established, but investigators have suggested that regulation of PKM2 activity can cause accumulation of glycolytic intermediates and increase flux through the pentose phosphate pathway. Recent evidence suggests that PKM2 also may have non-metabolic functions, including as a transcriptional co-activator in gene regulation. We reported previously that PKM2 is abundant in photoreceptor cells in mouse retinas...
February 14, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29441570/inhibition-of-nox4-dependent-ros-signaling-attenuates-prostate-fibroblast-activation-and-abrogates-stromal-mediated-pro-tumorigenic-interactions
#2
Natalie Sampson, Elena Brunner, Anja Weber, Martin Puhr, Georg Schäfer, Cedric Szyndralewiez, Helmut Klocker
Carcinoma-associated fibroblasts (CAFs) play a key onco-supportive role during prostate cancer (PCa) development and progression. We previously reported that the reactive oxygen species (ROS)-producing enzyme NADPH oxidase 4 (Nox4) is essential for TGFβ1-mediated activation of primary prostate human fibroblasts to a CAF-like phenotype. This study aimed to further investigate the functional relevance of prostatic Nox4 and determine whether pharmacological inhibition of stromal Nox4 abrogates paracrine-mediated PCa-relevant processes...
February 14, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29426376/silencing-of-nadph-oxidase-4-attenuates-hypoxia-resistance-in-neuroblastoma-cells-shsy-5y-by-inhibiting-pi3k-akt-dependent-glycolysis
#3
Ting Yu, Lei Li, Wenyan Liu, Bailiu Ya, Hongju Cheng, Qing Xin
Hypoxia-induced chemoresistance is a major obstacle in the development of effective cancer therapy. In our study, the reversal abilities of NADPH oxidase 4 (NOX4) silence on the hypoxia resistance and the potential mechanism were investigated. Our data showed that the expression of NOX4 was up-regulated in human neuroblastoma cells SHSY-5Y under hypoxia condition time-dependently. Knockdown of NOX4 expression by siRNA inhibited glycolysis induced by hypoxia through decreasing the expression of glycolysis related proteins (HIF-1α, LDHA, PDK1), decreasing glucose uptake, lactate production, ROS production while increasing mitochondria membrane potential...
February 9, 2018: Oncology Research
https://www.readbyqxmd.com/read/29416750/pharmacological-targeting-of-ros-reaction-network-in-myeloid-leukemia-cells-monitored-by-ultra-weak-photon-emission
#4
Rosilene Cristina Rossetto Burgos, Rawi Ramautar, Eduard P A Van Wijk, Thomas Hankemeier, Jan Van Der Greef, Alireza Mashaghi
Acute myeloid leukemia (AML) is a blood cancer that is caused by a disorder of the process that normally generates neutrophils. Function and dysfunction of neutrophils are key to physiologic defense against pathogens as well as pathologies including autoimmunity and cancer. A major mechanism through which neutrophils contribute to health and disease is oxidative burst, which involves rapid release of reactive oxygen species (ROS) generated by a chemical reaction network catalyzed by enzymes including NADPH oxidase and myeloperoxidase (MPO)...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29416728/crucial-role-of-pro-inflammatory-cytokines-from-respiratory-tract-upon-pm2-5-exposure-in-causing-the-bmscs-differentiation-in-cells-and-animals
#5
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
https://www.readbyqxmd.com/read/29413963/renal-protective-effect-of-polysulfide-in-cisplatin-induced-nephrotoxicity
#6
Xu Cao, Xiaowei Nie, Siping Xiong, Lei Cao, Zhiyuan Wu, Philip K Moore, Jin-Song Bian
Cisplatin is a major chemotherapeutic drug for solid tumors whereas it may lead to severe nephrotoxicity. Despite decades of efforts, effective therapies remain largely lacking for this disease. In the current research, we investigated the therapeutic effect of hydrogen polysulfide, a novel hydrogen sulfide (H2S) derived signaling molecule, in cisplatin nephrotoxicity and the mechanisms involved. Our results showed that polysulfide donor Na2S4 ameliorated cisplatin-caused renal toxicity in vitro and in vivo through suppressing intracellular reactive oxygen species (ROS) generation and downstream mitogen-activated protein kinases (MAPKs) activation...
February 1, 2018: Redox Biology
https://www.readbyqxmd.com/read/29413894/altered-metabolism-of-leukemic-cells-new-therapeutic-opportunity
#7
Julia Starkova, Ivana Hermanova, Katerina Hlozkova, Alzbeta Hararova, Jan Trka
The cancer metabolic program alters bioenergetic processes to meet the higher demands of tumor cells for biomass production, nucleotide synthesis, and NADPH-balancing redox homeostasis. It is widely accepted that cancer cells mostly utilize glycolysis, as opposed to normal cells, in which oxidative phosphorylation is the most employed bioenergetic process. Still, studies examining cancer metabolism had been overlooked for many decades, and it was only recently discovered that metabolic alterations affect both the oncogenic potential and therapeutic response...
2018: International Review of Cell and Molecular Biology
https://www.readbyqxmd.com/read/29410996/modulation-of-thiol-dependent-redox-system-by-metal-ions-via-thioredoxin-and-glutaredoxin-systems
#8
REVIEW
Yanfang Ouyang, Yi Peng, Jing Li, Arne Holmgren, Jun Lu
The thioredoxin and glutaredoxin systems possess a variety of biological activities in mammalian cells, including the defense against oxidative stress, regulation of DNA synthesis, the cell cycle and the mediation of apoptosis. The thioredoxin system, comprised of NADPH, thioredoxin reductase (TrxR) and thioredoxin (Trx), exerts its activities via a disulfide-dithiol exchange reaction. Mammalian TrxRs are selenoproteins; the thiols and selenols in the active site of these enzymes confer the thioredoxin system to work as soft bases, which have a high affinity with soft acids, including numerous metal ions...
February 7, 2018: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/29386184/lysophosphatidic-acid-induces-metabolic-reprogramming-in-ovarian-cancer-via-a-pseudohypoxic-response
#9
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
https://www.readbyqxmd.com/read/29374159/the-responsively-decreased-pkm2-facilitates-the-survival-of-pancreatic-cancer-cells-in-hypoglucose
#10
Xiang Li, Shichang Deng, Mingliang Liu, Yan Jin, Shuai Zhu, Shijiang Deng, Jingyuan Chen, Chi He, Qi Qin, Chunyou Wang, Gang Zhao
Cancer cells predominantly produce energy at a high rate of glycolysis even in aerobic environment. It is termed as Warburg effect and is necessary for the tumorigenesis. Studies showed pyruvate kinase M2 (PKM2), a key regulator of the Warburg effect, is overexpressed and involved in numerous cancers. However, the expression and function of PKM2 in pancreatic cancer (PC) remain undefined. Our results showed that PKM2 is overexpressed in the PC tissue compared to the peritumoral tissue. Unexpected, the downregulation of PKM2 did not affect the proliferation, invasion, and chemoresistance of PC cells...
January 26, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29361943/identification-of-danthron-as-an-isoform-specific-inhibitor-of-heme-oxygenase-1-cytochrome-p450-reductase-interaction-with-anti-tumor-activity
#11
Yi-Tai Chou, Fu-Fei Hsu, Dun-Yao Hu, Ying-Chih Chen, Yuan-Hao Hsu, John T-A Hsu, Lee-Young Chau
BACKGROUND: Heme oxygenase (HO) catalyzes NADPH-dependent degradation of heme to liberate iron, carbon monoxide and biliverdin. The interaction between HO and cytochrome P450 reductase (CPR), an electron donor, is essential for HO activity. HO-1 is a stress-inducible isoform whereas HO-2 is constitutively expressed. HO-1 induction is commonly seen in cancers and impacts disease progression, supporting the possibility of targeting HO-1 for cancer therapy. METHODS: We employed a cell-based bioluminescence resonance energy transfer assay to screen compounds with ability to inhibit HO-1/CPR interaction...
January 23, 2018: Journal of Biomedical Science
https://www.readbyqxmd.com/read/29355557/blockage-of-endoplasmic-reticulum-stress-attenuates-nilotinib-induced-cardiotoxicity-by-inhibition-of-the-akt-gsk3%C3%AE-nox4-signaling
#12
Qinghui Yang, Liang Wen, Zenghui Meng, Yanjun Chen
Cardiotoxicity is a critical side-effect of nilotinib during treatment for cancer, such as chronic myeloid leukemia, while the potential signaling mechanisms remain unclear. The role of and the relationship between endoplasmic reticulum (ER) stress and mitochondrial dysfunction was investigated in nilotinib-induced cardiac H9C2 injury as a suitable cell model. Our results showed that ER stress was persistently induced in nilotinib-treated cells, evidenced by increase of GRP78, CHOP, ATF4 and XBP1 as well as phospho-PERKThr980...
January 16, 2018: European Journal of Pharmacology
https://www.readbyqxmd.com/read/29352139/mitochondrial-glutamine-metabolism-via-got2-supports-pancreatic-cancer-growth-through-senescence-inhibition
#13
Seungyeon Yang, Sunsook Hwang, Minjoong Kim, Sung Bin Seo, Jeong-Hwa Lee, Seung Min Jeong
Cellular senescence, which leads to a cell cycle arrest of damaged or dysfunctional cells, is an important mechanism to restrain the malignant progression of cancer cells. Because metabolic changes underlie many cell-fate decisions, it has been suggested that cell metabolism might play key roles in senescence pathways. Here, we show that mitochondrial glutamine metabolism regulates senescence in human pancreatic ductal adenocarcinoma (PDAC) cells. Glutamine deprivation or inhibition of mitochondrial aspartate transaminase (GOT2) results in a profound induction of senescence and a suppression of PDAC growth...
January 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29331880/preventive-effects-of-indole-3-carbinol-against-alcohol-induced-liver-injury-in-mice-via-antioxidant-anti-inflammatory-and-anti-apoptotic-mechanisms-role-of-gut-liver-adipose-tissue-axis
#14
Youngshim Choi, Mohamed A Abdelmegeed, Byoung-Joon Song
Indole-3-carbinol (I3C), found in Brassica family vegetables, exhibits antioxidant, anti-inflammatory, and anti-cancerous properties. Here, we aimed to evaluate the preventive effects of I3C against ethanol (EtOH)-induced liver injury and study the protective mechanism(s) by using the well-established chronic-plus-binge alcohol exposure model. The preventive effects of I3C were evaluated by conducting various histological, biochemical, and real-time PCR analyses in mouse liver, adipose tissue, and colon, since functional alterations of adipose tissue and intestine can also participate in promoting EtOH-induced liver damage...
December 10, 2017: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/29323757/differentiation-associated-urothelial-cytochrome-p450-oxidoreductase-predicates-the-xenobiotic-metabolising-activity-of-luminal-muscle-invasive-bladder-cancers
#15
Simon C Baker, Volker M Arlt, Radek Indra, Madeleine Joel, Marie Stiborova, Ian Eardley, Niaz Ahmad, Wolfgang Otto, Maximilian Burger, Peter Rubenwolf, David H Phillips, Jennifer Southgate
Extra-hepatic metabolism of xenobiotics by epithelial tissues has evolved as a self-defence mechanism but has potential to contribute to the local activation of carcinogens. Bladder epithelium (urothelium) is bathed in excreted urinary toxicants and pro-carcinogens. This study reveals how differentiation affects cytochrome P450 (CYP) activity and the role of NADPH:P450 oxidoreductase (POR). CYP1A1 and CYP1B1 transcripts were inducible in normal human urothelial (NHU) cells maintained in both undifferentiated and functional barrier-forming differentiated states in vitro...
January 11, 2018: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/29321004/rcc2-over-expression-in-tumor-cells-alters-apoptosis-and-drug-sensitivity-by-regulating-rac1-activation
#16
Nan Wu, Dong Ren, Su Li, Wenli Ma, Shaoyan Hu, Yan Jin, Sheng Xiao
BACKGROUND: Small GTP binding protein Rac1 is a component of NADPH oxidases and is essential for superoxide-induced cell death. Rac1 is activated by guanine nucleotide exchange factors (GEFs), and this activation can be blocked by regulator of chromosome condensation 2 (RCC2), which binds the switch regions of Rac1 to prevent access from GEFs. METHODS: Three cancer cell lines with up- or down-regulation of RCC2 were used to evaluate cell proliferation, apoptosis, Rac1 signaling and sensitivity to a group of nine chemotherapeutic drugs...
January 10, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29320744/consumption-of-nadph-for-2-hg-synthesis-increases-pentose-phosphate-pathway-flux-and-sensitizes-cells-to-oxidative-stress
#17
Susan J Gelman, Fuad Naser, Nathaniel G Mahieu, Lisa D McKenzie, Gavin P Dunn, Milan G Chheda, Gary J Patti
Gain-of-function mutations in isocitrate dehydrogenase 1 (IDH1) occur in multiple types of human cancer. Here, we show that these mutations significantly disrupt NADPH homeostasis by consuming NADPH for 2-hydroxyglutarate (2-HG) synthesis. Cells respond to 2-HG synthesis, but not exogenous administration of 2-HG, by increasing pentose phosphate pathway (PPP) flux. We show that 2-HG production competes with reductive biosynthesis and the buffering of oxidative stress, processes that also require NADPH. IDH1 mutants have a decreased capacity to synthesize palmitate and an increased sensitivity to oxidative stress...
January 9, 2018: Cell Reports
https://www.readbyqxmd.com/read/29318449/reduction-oxidation-redox-system-in-radiation-induced-normal-tissue-injury-molecular-mechanisms-and-implications-in-radiation-therapeutics
#18
REVIEW
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
https://www.readbyqxmd.com/read/29317200/hyperuricemia-enhances-intracellular-urate-accumulation-via-down-regulation-of-cell-surface-bcrp-abcg2-expression-in-vascular-endothelial-cells
#19
Hisakazu Komori, Kazuyuki Yamada, Ikumi Tamai
Hyperuricemia has been recognized as an independent risk factor for cardiovascular disease. Urate stimulates NADPH oxidase and induces production of reactive oxygen species (ROS); consequently, intracellular urate accumulation can induce oxidative stress leading to endothelial dysfunction. Here, we studied the mechanism involved, using human umbilical vascular endothelial cells (HUVEC) as a model. Pretreatment with 15mg/dL unlabeled uric acid (corresponding to hyperuricemia) resulted in increased uptake of [14C]uric acid at steady-state by HUVEC, whereas pretreatment with 5mg/dL uric acid (in the normal serum concentration range) did not...
January 6, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29316804/renal-protective-effect-of-hydrogen-sulfide-in-cisplatin-induced-nephrotoxicity
#20
Xu Cao, Siping Xiong, Yebo Zhou, Zhi-Yuan Wu, Lei Ding, Yike Zhu, Mark Wood, Matthew Whiteman, Philip K Moore, Jin-Song Bian
AIMS: Cisplatin is a major therapeutic drug for solid tumors, but can cause severe nephrotoxicity. However, the role and therapeutic potential of hydrogen sulfide (H2S), an endogenous gaso-transmitter, in cisplatin-induced nephrotoxicity remains to be defined. RESULTS: Cisplatin led to the impairment of H2S production in vitro and in vivo by downregulating the expression level of cystathionine γ-lyase (CSE), which may contribute to the subsequent renal proximal tubule (RPT) cell death and thereby renal toxicity...
January 9, 2018: Antioxidants & Redox Signaling
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