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https://www.readbyqxmd.com/read/29656218/improved-hypocrellin-a-production-in-shiraia-bambusicola-by-light-dark-shift
#1
Chun Xiao Sun, Yan Jun Ma, Jian Wen Wang
Hypocrellin A (HA) is a major bioactive perylenequinone from the fruiting body of Shiraia bambusicola used for the treatment of skin diseases and developed as a photodynamic therapy (PDT) agent against cancers and viruses. The mycelial culture of S. bambusicola under dark is a biotechnological alternative for HA production but with low yield. In this study, light and dark conditions were investigated to develop effective elicitation on HA production in the cultures. Our results showed the constant light at 200 lx stimulated HA production without any growth retardation of mycelia...
April 9, 2018: Journal of Photochemistry and Photobiology. B, Biology
https://www.readbyqxmd.com/read/29651790/novel-insights-for-inhibiting-mutant-heterodimer-idh1-wt-r132h-in-cancer-an-in-silico-approach
#2
Ezequiel Iván Juritz, Juan Pablo Bascur, Daniel Eduardo Almonacid, Fernando Danilo González-Nilo
BACKGROUND: Isocitrate dehydrogenase 1 (IDH1) is a dimeric enzyme responsible for supplying the cell's nicotinamide adenine dinucleotide phosphate (NADPH) reserves via dehydrogenation of isocitrate (ICT) and reduction of NADP+. Mutations in position R132 trigger cancer by enabling IDH1 to produce D-2-hydroxyglutarate (2-HG) and reduce inhibition by ICT. Mutant IDH1 can be found as a homodimer or a heterodimer. OBJECTIVE: We propose a novel strategy to inhibit IDH1 R132 variants as a means not to decrease the concentration of 2-HG but to provoke a cytotoxic effect, as the cell malignancy at this point no longer depends on 2-HG...
April 12, 2018: Molecular Diagnosis & Therapy
https://www.readbyqxmd.com/read/29617059/aldo-keto-reductases-mediated-cytotoxicity-of-2-deoxyglucose-a-novel-anticancer-mechanism
#3
Shi-Qing Zhang, Kin-Lam Ken Yung, Sookja Kim Chung, Sum-Man Stephen Chung
2-Deoxyglucose is a non-metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. It is thought to preferentially kill cancer cells by inhibiting glycolysis because cancer cells are more dependent on glycolysis for their energy needs than normal cells. However, we found that 2-Deoxyglucose's toxicity in cancer cells is mediated by the enzymatic activities of AKR1B1 and/or AKR1B10 (AKR1Bs), which are often overexpressed in cancer cells...
April 4, 2018: Cancer Science
https://www.readbyqxmd.com/read/29601126/expression-of-cytosolic-malic-enzyme-me1-is-associated-with-disease-progression-in-human-oral-squamous-cell-carcinoma
#4
Chie Nakashima, Kazuhiko Yamamoto, Rina Fujiwara-Tani, Yi Luo, Sayako Matsushima, Kiyomu Fujii, Hitoshi Ohmori, Tomonori Sasahira, Takamitsu Sasaki, Yasuhiko Kitadai, Tadaaki Kirita, Hiroki Kuniyasu
Malic enzyme 1 (ME1) is a multifunctional protein involved in glycolysis, the citric acid cycle, NADPH production, glutamine metabolism, and lipogenesis. It is overexpressed in various cancers. We examined the expression of ME1 in 119 oral squamous cell carcinomas (OSCCs) via immunohistochemistry. ME1 expression was moderate to strong expression in 57 (48%) OSCCs and correlated with pT, pN, clinical stage, and histological grade. In 37 cases with prognostic evaluation, moderate to strong ME1 expression indicated a worse prognosis than did weak ME1 expression...
March 30, 2018: Cancer Science
https://www.readbyqxmd.com/read/29599747/circadian-and-metabolic-perspectives-in-the-role-played-by-nadph-in-cancer
#5
REVIEW
Isabel Méndez, Mauricio Díaz-Muñoz
Physiological activity in healthy conditions requires a coordinated interaction between the molecular circadian clock and the network of biochemical pathways. An important metabolic parameter in the interface between these two entities is the redox state. Among the redox coenzymes that regulate the fluxes of enzymatic reactions is the NADP+ /NADPH pair. Indeed, the main biosynthetic pathways need NADPH to serve as an electron donor for cellular anabolic transformations. The existence of a metabolic circadian clock is well established, and it was first identified in mammalian red blood cells...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29570984/effects-of-the-green-tea-polyphenol-epigallocatechin-3-gallate-on-glioma-a-critical-evaluation-of-the-literature
#6
Chung T Le, William P J Leenders, Remco J Molenaar, Cornelis J F van Noorden
The review discusses the effects of Epigallocatechin-3-gallate Gallate (EGCG) on glioma as a basis for future research on clinical application of EGCG. Epidemiological studies on the effects of green tea or EGCG on the risk of glioma is inconclusive due to the limited number of studies, the inclusion of all tea types in these studies, and the focus on caffeine rather than EGCG. In vivo experiments using EGCG monotherapy are inconclusive. Nevertheless, EGCG induces cell death, prevents cellular proliferation, and limits invasion in multiple glioma cell lines...
March 23, 2018: Nutrition and Cancer
https://www.readbyqxmd.com/read/29548337/the-interplay-of-reactive-oxygen-species-and-the-epidermal-growth-factor-receptor-in-tumor-progression-and-drug-resistance
#7
REVIEW
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
https://www.readbyqxmd.com/read/29545180/hepatic-glucose-6-phosphatase-%C3%AE-deficiency-leads-to-metabolic-reprogramming-in-glycogen-storage-disease-type-ia
#8
Jun-Ho Cho, Goo-Young Kim, Brian C Mansfield, Janice Y Chou
Glycogen storage disease type Ia (GSD-Ia) is caused by a deficiency in glucose-6-phosphatase-α (G6Pase-α or G6PC), a key enzyme in endogenous glucose production. This autosomal recessive disorder is characterized by impaired glucose homeostasis and long-term complications of hepatocellular adenoma/carcinoma (HCA/HCC). We have shown that hepatic G6Pase-α deficiency-mediated steatosis leads to defective autophagy that is frequently associated with carcinogenesis. We now show that hepatic G6Pase-α deficiency also leads to enhancement of hepatic glycolysis and hexose monophosphate shunt (HMS) that can contribute to hepatocarcinogenesis...
March 12, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29544379/the-effect-of-carbon-irradiation-is-associated-with-greater-oxidative-stress-in-mouse-intestine-and-colon-relative-to-%C3%AE-rays
#9
Shubhankar Suman, Santosh Kumar, Albert J Jr Fornace, Kamal Datta
Carbon irradiation due to its higher biological effectiveness relative to photon radiation is a concern for toxicity to proliferative normal gastrointestinal (GI) tissue after radiotherapy and long-duration space missions such as mission to Mars. Although radiation-induced oxidative stress is linked to chronic diseases such as cancer, effects of carbon irradiation on normal GI tissue have not been fully understood. This study assessed and compared chronic oxidative stress in mouse intestine and colon after different doses of carbon and γ radiation, which are qualitatively different...
March 16, 2018: Free Radical Research
https://www.readbyqxmd.com/read/29534964/inhibiting-6-phosphogluconate-dehydrogenase-reverses-doxorubicin-resistance-in-anaplastic-thyroid-cancer-via-inhibiting-nadph-dependent-metabolic-reprogramming
#10
Ling Ma, Qiao Cheng
Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid malignancies and resistant to chemotherapy. Little is known on the underlying mechanisms of ATC resistance to chemotherapy. In our work, we identified that 6-phosphogluconate dehydrogenase (6PGD) is critically involved in the development of ATC resistance to doxorubicin. We found that 6PGD mRNA, protein and enzyme activity levels are significantly upregulated in ATC cells during the prolonged exposure to doxorubicin in a time-dependent manner...
March 10, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29531162/-lnc-chop-promotes-immunosuppressive-function-of-myeloid-derived-suppressor-cells-in-tumor-and-inflammatory-environments
#11
Yunhuan Gao, Tiantian Wang, Yuanyuan Li, Yuan Zhang, Rongcun Yang
Myeloid-derived suppressor cells (MDSCs) are major regulators of immune responses in cancer. Both C/EBP homologous protein (CHOP) and C/EBPβ play a critical role in regulating immunosuppressive function of MDSCs. In this study, we identified a novel long noncoding RNA termed as lnc-chop in MDSCs, which may interact with CHOP and the C/EBPβ isoform liver-enriched inhibitory protein. The binding of lnc-chop with both CHOP and the C/EBPβ isoform liver-enriched inhibitory protein promoted the activation of C/EBPβ and upregulated the expression of arginase-1, NO synthase 2, NADPH oxidase 2, and cyclooxygenase-2, which are related to the immunosuppressive function of MDSCs in inflammatory and tumor environments...
March 12, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29513521/the-double-edged-sword-profile-of-redox-signaling-oxidative-events-as-molecular-switches-in-the-balance-between-cell-physiology-and-cancer
#12
Sonia Emanuele, Antonella D'Anneo, Giuseppe Calvaruso, Cesare Cernigliaro, Michela Giuliano, Marianna Lauricella
The intracellular redox state in the cell depends on the balance between the level of reactive oxygen species (ROS) and the activity of defensive systems including antioxidant enzymes. This balance is a dynamic process that can change in relation to many factors and/or stimuli induced within the cell. ROS production is derived from physiological metabolic events. For instance, mitochondria represent the major ROS sources during oxidative phosphorylation, but other systems, such as NADPH oxidase or specific enzymes in certain metabolisms, may account for ROS production as well...
March 7, 2018: Chemical Research in Toxicology
https://www.readbyqxmd.com/read/29502733/metformin-prevention-of-genomic-instability-and-cancer-a-review
#13
Masoud Najafi, Mohsen Cheki, Saeed Rezapoor, Ghazale Geraily, Elahe Motevaseli, Carla Carnovale, Emilio Clementi, Alireza Shirazi
The diabetes drug metformin can mitigate the genotoxic effects of cytotoxic agents and has been proposed to prevent or even cure certain cancers. Metformin reduces DNA damage by mechanisms that are only incompletely understood. Metformin scavenges free radicals, including reactive oxygen species and nitric oxide, which are produced by genotoxicants such as ionizing or non-ionizing radiation, heavy metals, and chemotherapeutic agents. The drug may also increase the activities of antioxidant enzymes and inhibit NADPH oxidase, cyclooxygenase-2, and inducible nitric oxide synthase, thereby limiting macrophage recruitment and inflammatory responses...
March 2018: Mutation Research
https://www.readbyqxmd.com/read/29496628/nox4-driven-ros-formation-regulates-proliferation-and-apoptosis-of-gastric-cancer-cells-through-the-gli1-pathway
#14
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
https://www.readbyqxmd.com/read/29478325/carcinogenesis-and-ros-signaling-interaction-of-the-nadph-oxidase-nox1-5-and-superoxide-dismutase-1-3-signal-transduction-pathways
#15
Alessia Parascandolo, Mikko Laukkanen
Reduction oxidation (redox) balance could be defined as an even distribution of reduction and oxidation complementary processes and their reaction end products. There is a consensus that aberrant levels of reactive oxygen species (ROS), commonly observed in cancer, stimulate primary cell immortalization and progression of carcinogenesis. However, mechanism how different ROS regulate redox balance is not completely understood. In the current review, we have summarized the main signaling cascades inducing NADPH oxidase NOX1-5 and SOD1-3 expression and their connection to cell proliferation, immortalization, transformation, and CD34+ cell differentiation in thyroid, colon, lung, breast, and hematological cancers...
February 24, 2018: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29471502/elevated-g6pd-expression-contributes-to-migration-and-invasion-of-hepatocellular-carcinoma-cells-by-inducing-epithelial-mesenchymal-transition
#16
Ming Lu, Lu Lu, Qiongzhu Dong, Guangyang Yu, Jinhong Chen, Lunxiu Qin, Lianxin Wang, Wenwei Zhu, Huliang Jia
Altered metabolism is one of the hallmarks of cancer cells. Pentose phosphate pathway (PPP) is a fundamental component of cellular metabolism. Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the PPP, is elevated in many cancers and contributes to tumor growth by producing ribose-5-phosphate and NADPH through PPP. However, the role of G6PD in hepatocellular carcinoma (HCC) metastasis and the clinical significance of G6PD in HCC progression and prognosis have not been well determined. In this study, by investigating tissue samples from HCC patients and HCC cell lines, we found that elevated G6PD expression is significantly associated with HCC metastasis and poor prognosis of HCCs, and that knockdown of G6PD inhibits in vitro proliferation, migration and invasion of HCC cell lines...
February 17, 2018: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/29459781/ripk1-mediated-induction-of-mitophagy-compromises-the-viability-of-extracellular-matrix-detached-cells
#17
Mark A Hawk, Cassandra L Gorsuch, Patrick Fagan, Chan Lee, Sung Eun Kim, Jens C Hamann, Joshua A Mason, Kelsey J Weigel, Matyas Abel Tsegaye, Luqun Shen, Sydney Shuff, Junjun Zuo, Stephan Hu, Lei Jiang, Sarah Chapman, W Matthew Leevy, Ralph J DeBerardinis, Michael Overholtzer, Zachary T Schafer
For cancer cells to survive during extracellular matrix (ECM) detachment, they must inhibit anoikis and rectify metabolic deficiencies that cause non-apoptotic cell death. Previous studies in ECM-detached cells have linked non-apoptotic cell death to reactive oxygen species (ROS) generation, although the mechanistic underpinnings of this link remain poorly defined. Here, we uncover a role for receptor-interacting protein kinase 1 (RIPK1) in the modulation of ROS and cell viability during ECM detachment. We find that RIPK1 activation during ECM detachment results in mitophagy induction through a mechanism dependent on the mitochondrial phosphatase PGAM5...
March 2018: Nature Cell Biology
https://www.readbyqxmd.com/read/29456845/low-carbonyl-reductase-1-expression-is-associated-with-poor-prognosis-in-patients-with-oral-squamous-cell-carcinoma
#18
Ryota Yamanouchi, Koji Harada, Tarannum Ferdous, Yoshiya Ueyama
Carbonyl reductase 1 (CBR1) is an enzyme that catalyzes the reduction of numerous compounds by using NADPH-dependent oxidoreductase activity. Decreased expression of CBR1 is associated with disease progression and an unfavorable outcome in several types of malignancies. The purpose of the current study was to determine whether CBR1 expression could be a useful prognostic factor in patients with oral squamous cell carcinoma (OSCC). Therefore, its mechanisms of action were investigated in order to understand how CBR1 affects cancer cell behavior in vitro ...
March 2018: Molecular and Clinical Oncology
https://www.readbyqxmd.com/read/29445082/pyruvate-kinase-m2-regulates-photoreceptor-structure-function-and-viability
#19
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
#20
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
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