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https://www.readbyqxmd.com/read/28208702/the-glutamate-dehydrogenase-pathway-and-its-roles-in-cell-and-tissue-biology-in-health-and-disease
#1
REVIEW
Andreas Plaitakis, Ester Kalef-Ezra, Dimitra Kotzamani, Ioannis Zaganas, Cleanthe Spanaki
Glutamate dehydrogenase (GDH) is a hexameric enzyme that catalyzes the reversible conversion of glutamate to α-ketoglutarate and ammonia while reducing NAD(P)⁺ to NAD(P)H. It is found in all living organisms serving both catabolic and anabolic reactions. In mammalian tissues, oxidative deamination of glutamate via GDH generates α-ketoglutarate, which is metabolized by the Krebs cycle, leading to the synthesis of ATP. In addition, the GDH pathway is linked to diverse cellular processes, including ammonia metabolism, acid-base equilibrium, redox homeostasis (via formation of fumarate), lipid biosynthesis (via oxidative generation of citrate), and lactate production...
February 8, 2017: Biology
https://www.readbyqxmd.com/read/28196727/nrf2-mediates-redox-adaptation-in-nox4-overexpressed-non-small-cell-lung-cancer-cells
#2
Qipeng Wu, Bei Yao, Ning Li, Lei Ma, Yanchao Deng, Yang Yang, Cheng Zeng, Zhicheng Yang, Bing Liu
The redox adaptation mechanisms in cancer cells are very complex and remain largely unclear. Our previous studies have confirmed that NADPH oxidase 4 (NOX4) is abundantly expressed in non-small cell lung cancer (NSCLC) and confers apoptosis resistance on NSCLC cells. However, the comprehensive mechanisms for NOX4-mediated oxidative resistance of cancer cells remain still undentified. The present study found that NOX4-derived H2O2 enhanced the nuclear factor erythroid 2-related factor 2 (Nrf2) stability via disruption of redox-dependent proteasomal degradation and stimulated its activity through activation of PI3K signaling...
February 11, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28191009/defective-il-23-il-17-axis-protects-p47phox-mice-from-colon-cancer
#3
Cornelia Richter, Martina Herrero San Juan, Benno Weigmann, Dominik Bergis, Katrin Dauber, Michael H Muders, Gustavo B Baretton, Josef Martin Pfeilschifter, Halvard Bonig, Sebastian Brenner, Heinfried H Radeke
In the colon, a sophisticated balance between immune reaction and tolerance is absolutely required. Dysfunction may lead to pathologic phenotypes ranging from chronic inflammatory processes to cancer development. Two prominent modulators of colon inflammation are represented by the closely related cytokines interleukin (IL)-12 and IL-23, which initiate adaptive Th1 and Th17 immune responses, respectively. In this study, we investigated the impact of the NADPH oxidase protein p47phox, which negatively regulates IL-12 in dendritic cells, on colon cancer development in a colitis-associated colon cancer model...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28176759/snail-reprograms-glucose-metabolism-by-repressing-phosphofructokinase-pfkp-allowing-cancer-cell-survival-under-metabolic-stress
#4
Nam Hee Kim, Yong Hoon Cha, Jueun Lee, Seon-Hyeong Lee, Ji Hye Yang, Jun Seop Yun, Eunae Sandra Cho, Xianglan Zhang, Miso Nam, Nami Kim, Young-Su Yuk, So Young Cha, Yoonmi Lee, Joo Kyung Ryu, Sunghyouk Park, Jae-Ho Cheong, Sang Won Kang, Soo-Youl Kim, Geum-Sook Hwang, Jong In Yook, Hyun Sil Kim
Dynamic regulation of glucose flux between aerobic glycolysis and the pentose phosphate pathway (PPP) during epithelial-mesenchymal transition (EMT) is not well-understood. Here we show that Snail (SNAI1), a key transcriptional repressor of EMT, regulates glucose flux toward PPP, allowing cancer cell survival under metabolic stress. Mechanistically, Snail regulates glycolytic activity via repression of phosphofructokinase, platelet (PFKP), a major isoform of cancer-specific phosphofructokinase-1 (PFK-1), an enzyme involving the first rate-limiting step of glycolysis...
February 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28149332/the-immunomodulatory-anticancer-agent-rrx-001-induces-an-interferon-response-through-epigenetic-induction-of-viral-mimicry
#5
Hongjuan Zhao, Shoucheng Ning, Rosalie Nolley, Jan Scicinski, Bryan Oronsky, Susan J Knox, Donna M Peehl
BACKGROUND: RRx-001, a dinitroazetidine derivative, is a novel anticancer agent currently in phase II clinical trials. It mediates immunomodulatory effects either directly through polarization of tumor associated macrophages or indirectly through vascular normalization and increased T-lymphocyte infiltration. With multiple additional mechanisms of action including upregulation of oxidative stress, depletion of GSH and NADPH, anti-angiogenesis and epigenetic modulation, RRx-001 is being studied as a radio- and chemo-sensitizer to resensitize tumors to prior therapy and to prime tumors to respond to radiation, chemotherapy and immunotherapy in combination therapy studies...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/28143649/crosstalk-between-calcium-and-reactive-oxygen-species-signaling-in-cancer
#6
REVIEW
Nadine Hempel, Mohamed Trebak
The interplay between Ca(2+) and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca(2+) channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca(2+) signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca(2+) and ROS are important mediators of cell death...
January 18, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28132856/nadph-oxidase-1-plays-a-key-role-in-keratinocyte-responses-to-ultraviolet-radiation-and-uvb-induced-skin-carcinogenesis
#7
Houssam Raad, Martin Serrano-Sanchez, Ghida Harfouche, Walid Mahfouf, Doriane Bortolotto, Vanessa Bergeron, Zeinab Kasraian, Lea Dousset, Mohsen Hosseini, Alain Taieb, Hamid Reza Rezvani
The NADPH oxidase (NOX) family enzymes are involved in several physiological functions. However, their roles in keratinocyte responses to ultraviolet (UV) radiation have not been clearly elucidated. This study demonstrates that, among other NOX family members, UVB irradiation results in a biphasic activation of NOX1 that plays a critical role in defining keratinocyte fate through the modulation of the DNA damage response (DDR) network. Indeed, suppression of both bursts of UVB-induced NOX1 activation by using a specific peptide inhibitor of NOX1 (InhNOX1) is associated with increased nucleotide excision repair (NER) efficiency and reduction of apoptosis, which is finally translated into decreased photocarcinogenesis...
January 26, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28126350/peptostreptococcus-anaerobius-induces-intracellular-cholesterol-biosynthesis-in-colon-cells-to-induce-proliferation-and-causes-dysplasia-in-mice
#8
Ho Tsoi, Eagle Sh Chu, Xiang Zhang, Jianqiu Sheng, Daniel Nakatsu, Siew C Ng, Anthony Wh Chan, Francis Kl Chan, Joseph Jy Sung, Jun Yu
BACKGROUND & AIMS: Stool samples from patients with colorectal cancer (CRC) have a higher abundance of Peptostreptococcus anaerobius than stool from individuals without CRC, based on metagenome sequencing. We investigated whether P anaerobius contributes to colon tumor formation in mice and its possible mechanisms of carcinogenesis. METHODS: We performed quantitative PCR analyses to measure P anaerobius in 112 stool samples and 255 colon biopsies from patients with CRC or advanced adenoma and from healthy individuals (controls) undergoing colonoscopy examination at hospitals in Hong Kong and Beijing...
January 23, 2017: Gastroenterology
https://www.readbyqxmd.com/read/28122174/synthesis-qsar-studies-and-metabolic-stability-of-novel-2-alkylthio-4-chloro-n-5-oxo-4-5-dihydro-1-2-4-triazin-3-yl-benzenesulfonamide-derivatives-as-potential-anticancer-and-apoptosis-inducing-agents
#9
Beata Żołnowska, Jarosław Sławiński, Aneta Pogorzelska, Krzysztof Szafrański, Anna Kawiak, Grzegorz Stasiłojć, Mariusz Belka, Joanna Zielińska, Tomasz Bączek
A series of novel 2-alkylthio-4-chloro-N-(5-oxo-4,5-dihydro-1,2,4-triazin-3-yl)benzenesulfonamide derivatives 12-46 have been synthesized by the reaction of aminoguanidines with an appropriate alpha-oxo-acids hydrates in glacial acetic acid. All the synthesized compounds were evaluated for their anticancer activity against HeLa, HCT-116 and MCF-7 human tumor cell lines. Two compounds 33 and 34 displayed outstanding cytotoxic effect selectively toward HeLa cancer cells (IC50 = 19 μM) and did not exhibit toxicity to the non-cancerous HaCaT cells...
January 25, 2017: Chemical Biology & Drug Design
https://www.readbyqxmd.com/read/28111134/aldose-reductase-akr1b-deficiency-promotes-phagocytosis-in-bone-marrow-derived-mouse-macrophages
#10
Mahavir Singh, Aniruddh Kapoor, James McCracken, Bradford Hill, Aruni Bhatnagar
Macrophages are critical drivers of the immune response during infection and inflammation. The pathogenesis of several inflammatory conditions, such as diabetes, cancer and sepsis has been linked with aldose reductase (AR), a member of the aldo-keto reductase (AKR) superfamily. However, the role of AR in the early stages of innate immunity such as phagocytosis remains unclear. In this study, we examined the role of AR in regulating the growth and the phagocytic activity of bone marrow-derived mouse macrophages (BMMs) from AR-null and wild-type (WT) mice...
January 19, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28102848/statins-in-anthracycline-induced-cardiotoxicity-rac-and-rho-and-the-heartbreakers
#11
REVIEW
Christian Henninger, Gerhard Fritz
Cancer patients receiving anthracycline-based chemotherapy are at risk to develop life-threatening chronic cardiotoxicity with the pathophysiological mechanism of action not fully understood. Besides the most common hypothesis that anthracycline-induced congestive heart failure (CHF) is mainly caused by generation of reactive oxygen species, recent data point to a critical role of topoisomerase II beta (TOP2B), which is a primary target of anthracycline poisoning, in the pathophysiology of CHF. As the use of the only clinically approved cardioprotectant dexrazoxane has been limited by the FDA in 2011, there is an urgent need for alternative cardioprotective measures...
January 19, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28101244/celery-extract-inhibits-mouse-cyp2a5-and-human-cyp2a6-activities-via-different-mechanisms
#12
Xiao Deng, Qianghong Pu, Erhao Wang, Chao Yu
Human cytochrome P450 (CYP) 2A6 participates in the metabolism of nicotine and precarcinogens, thus the deliberate inhibition of CYP2A6 may reduce cigarette consumption and therefore reduce the risk of developing the types of cancer associated with smoking. The inhibitory effects and mechanisms of celery (Apium graveolens) extract on mouse CYP2A5 and human CYP2A6 activity remain unclear. These effects were investigated in mouse and human liver microsomes using coumarin 7-hydroxylation in a probe reaction. Celery extract reduced CYP2A5 and CYP2A6 activities in vitro in a dose-dependent manner...
December 2016: Oncology Letters
https://www.readbyqxmd.com/read/28099419/genomic-deletion-of-malic-enzyme-2-confers-collateral-lethality-in-pancreatic-cancer
#13
Prasenjit Dey, Joelle Baddour, Florian Muller, Chia Chin Wu, Huamin Wang, Wen-Ting Liao, Zangdao Lan, Alina Chen, Tony Gutschner, Yaan Kang, Jason Fleming, Nikunj Satani, Di Zhao, Abhinav Achreja, Lifeng Yang, Jiyoon Lee, Edward Chang, Giannicola Genovese, Andrea Viale, Haoqiang Ying, Giulio Draetta, Anirban Maitra, Y Alan Wang, Deepak Nagrath, Ronald A DePinho
The genome of pancreatic ductal adenocarcinoma (PDAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homozygously deleted in nearly one-third of cases. As loss of neighbouring housekeeping genes can confer collateral lethality, we sought to determine whether loss of the metabolic gene malic enzyme 2 (ME2) in the SMAD4 locus would create cancer-specific metabolic vulnerability upon targeting of its paralogous isoform ME3. The mitochondrial malic enzymes (ME2 and ME3) are oxidative decarboxylases that catalyse the conversion of malate to pyruvate and are essential for NADPH regeneration and reactive oxygen species homeostasis...
February 2, 2017: Nature
https://www.readbyqxmd.com/read/28098862/rhein-suppresses-matrix-metalloproteinase-production-by-regulating-the-rac1-ros-mapk-ap-1-pathway-in-human-ovarian-carcinoma-cells
#14
Guomei Zhou, Fenghui Peng, Yanping Zhong, Yanhua Chen, Min Tang, Danrong Li
Matrix metalloproteinases (MMPs) are a family of calcium-dependent zinc-containing endopeptidases, which play an integral role in migration and invasion of ovarian cancer. Rac1 proteins might mostly influence cell migration and invasion by generating endogenous reactive oxygen species. Therefore, inhibiting MMPs and regulating the Rac1/ROS/MAPK/AP-1 pathway may be a new therapeutic strategy for ovarian cancer. In this study, we found that rhein could suppress the invasion and migration of SKOV3-PM4 cells with characteristics of directional highly lymphatic metastasis...
March 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28092678/6-phosphofructo-2-kinase-fructose-2-6-biphosphatase-4-is-essential-for-p53-null-cancer-cells
#15
S Ros, J Flöter, I Kaymak, C Da Costa, A Houddane, S Dubuis, B Griffiths, R Mitter, S Walz, S Blake, A Behrens, K M Brindle, N Zamboni, M H Rider, A Schulze
The bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-4 (PFKFB4) controls metabolic flux through allosteric regulation of glycolysis. Here we show that p53 regulates the expression of PFKFB4 and that p53-deficient cancer cells are highly dependent on the function of this enzyme. We found that p53 downregulates PFKFB4 expression by binding to its promoter and mediating transcriptional repression via histone deacetylases. Depletion of PFKFB4 from p53-deficient cancer cells increased levels of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolytic activity but decreased routing of metabolites through the oxidative arm of the pentose-phosphate pathway...
January 16, 2017: Oncogene
https://www.readbyqxmd.com/read/28081539/regulation-of-anoikis-resistance-by-nadph-oxidase-4-and-epidermal-growth-factor-receptor
#16
Hyeryeong Kim, Jee Young Sung, Eun-Kyung Park, Seongho Kho, Kyung Hee Koo, Seog-Yun Park, Sung-Ho Goh, Yoon Kyung Jeon, Sekyung Oh, Byung-Kiu Park, Yong-Keun Jung, Yong-Nyun Kim
BACKGROUND: Normal cells are sensitive to anoikis, which is a cell detachment-induced apoptosis. However, cancer cells acquire anoikis resistance that is essential for successful metastasis. This study aimed to demonstrate the function and potential mechanism of NADPH oxidase 4 (NOX4) and EGFR activation in regulating anoikis resistance in lung cancer. METHODS: Cells were cultured either in the attached or suspended condition. Cell viability was measured by cell counting and live and dead cell staining...
January 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28076881/constitutive-nos-uncoupling-and-nadph-oxidase-upregulation-in-the-penis-of-type-2-diabetic-men-with-erectile-dysfunction
#17
B Musicki, A L Burnett
Erectile dysfunction (ED) associated with type 2 diabetes mellitus (T2DM) involves dysfunctional nitric oxide (NO) signaling and increased oxidative stress in the penis. However, the mechanisms of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS) dysregulation, and the sources of oxidative stress, are not well defined, particularly at the human level. The objective of this study was to define whether uncoupled eNOS and nNOS, and NADPH oxidase upregulation, contribute to the pathogenesis of ED in T2DM men...
January 11, 2017: Andrology
https://www.readbyqxmd.com/read/28069826/endostatin-inhibits-androgen-independent-prostate-cancer-growth-by-suppressing-nuclear-receptor-mediated-oxidative-stress
#18
Joo Hyoung Lee, Minsung Kang, Hong Wang, Gurudatta Naik, James A Mobley, Guru Sonpavde, W Timothy Garvey, Victor M Darley-Usmar, Selvarangan Ponnazhagan
Androgen-deprivation therapy has been identified to induce oxidative stress in prostate cancer (PCa), leading to reactivation of androgen receptor (AR) signaling in a hormone-refractory manner. Thus, antioxidant therapies have gained attention as adjuvants for castration-resistant PCa. Here, we report for the first time that human endostatin (ES) prevents androgen-independent growth phenotype in PCa cells through its molecular targeting of AR and glucocorticoid receptor (GR) and downstream pro-oxidant signaling...
January 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28069379/ndrg2-overexpression-suppresses-hepatoma-cells-survival-during-metabolic-stress-through-disturbing-the-activation-of-fatty-acid-oxidation
#19
Tao Pan, Mei Zhang, Fang Zhang, Guang Yan, Yi Ru, Qinhao Wang, Yao Zhang, Xuehui Wei, Xinyuan Xu, Lan Shen, Jian Zhang, Kaichun Wu, Libo Yao, Xia Li
Because of the high nutrient consumption and inadequate vascularization, solid tumor constantly undergoes metabolic stress during tumor development. Oncogenes and tumor suppressor genes participated in cancer cells' metabolic reprogramming. N-Myc downstream regulated gene 2 (NDRG2) is a recently identified tumor suppressor gene, but its function in cancer metabolism, particularly during metabolic stress, remains unclear. In this study, we found that NDRG2 overexpression significantly reduced hepatoma cell proliferation and enhanced cell apoptosis under glucose limitation...
January 7, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28063379/oxidative-stress-mitochondrial-abnormalities-and-antioxidant-defense-in-ataxia-telangiectasia-bloom-syndrome-and-nijmegen-breakage-syndrome
#20
REVIEW
Mateusz Maciejczyk, Bozena Mikoluc, Barbara Pietrucha, Edyta Heropolitanska-Pliszka, Malgorzata Pac, Radosław Motkowski, Halina Car
Rare pleiotropic genetic disorders, Ataxia-telangiectasia (A-T), Bloom syndrome (BS) and Nijmegen breakage syndrome (NBS) are characterised by immunodeficiency, extreme radiosensitivity, higher cancer susceptibility, premature aging, neurodegeneration and insulin resistance. Some of these functional abnormalities can be explained by aberrant DNA damage response and chromosomal instability. It has been suggested that one possible common denominator of these conditions could be chronic oxidative stress caused by endogenous ROS overproduction and impairment of mitochondrial homeostasis...
December 28, 2016: Redox Biology
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