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NAD+ AND cancer

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https://www.readbyqxmd.com/read/28537923/aldehyde-dehydrogenase-1a1-increases-nadh-levels-and-promotes-tumor-growth-via-glutathione-dihydrolipoic-acid-dependent-nad-reduction
#1
Baiyun Wang, Xue Chen, Zixi Wang, Wei Xiong, Tao Xu, Xinyuan Zhao, Yang Cao, Yanru Guo, Lin Li, She Chen, Song Huang, Xiaodong Wang, Min Fang, Zhirong Shen
Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD+ to NADH. We report here that ALDH1A1 can also use glutathione (GSH) and dihydrolipoic acid (DHLA) as electron donors to reduce NAD+ to NADH. The GSH/DHLA-dependent NAD+-reduction activity of ALDH1A1 is not affected by the aldehyde dehydrogenase inhibitor or by mutation of the residues in its aldehyde-binding pocket...
May 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28529598/biological-interaction-of-cigarette-smoking-on-the-association-between-genetic-polymorphisms-involved-in-inflammation-and-the-risk-of-lung-cancer-a-case-control-study-in-japan
#2
Yuzo Yamamoto, Chikako Kiyohara, Saiko Suetsugu-Ogata, Naoki Hamada, Yoichi Nakanishi
Chronic inflammation serves an important role in lung carcinogenesis, thus genetic polymorphisms involved in this pathway may affect the risk of lung cancer. The present case-control study focused on the association between lung cancer risk and genetic polymorphisms involved in inflammatory pathways. The study comprised 462 lung cancer cases and 379 controls from Japan. The roles of interleukin 8 (IL8) rs4073, nuclear factor kappa B (NFκB) rs28362491, cytochrome b-245, alpha polypeptide (CYBA) rs4673, NAD(P) H dehydrogenase, quinone 1 (NQO1) rs1800566, nitric oxide synthase 2 and inducible (NOS2) rs2297518 polymorphisms in lung carcinogenesis were investigated...
May 2017: Oncology Letters
https://www.readbyqxmd.com/read/28527050/interplay-between-sirt-3-metabolism-and-its-tumor-suppressor-role-in-hepatocellular-carcinoma
#3
REVIEW
Serena De Matteis, Anna Maria Granato, Roberta Napolitano, Chiara Molinari, Martina Valgiusti, Daniele Santini, Francesco Giuseppe Foschi, Giorgio Ercolani, Umberto Vespasiani Gentilucci, Luca Faloppi, Mario Scartozzi, Giovanni Luca Frassineti, Andrea Casadei Gardini
Sirtuins (SIRT), first described as nicotinamide adenine dinucleotide (NAD(+))-dependent type III histone deacetylases, are produced by cells to support in the defense against chronic stress conditions such as metabolic syndromes, neurodegeneration, and cancer. SIRT-3 is one of the most studied members of the mitochondrial sirtuins family. In particular, its involvement in metabolic diseases and its dual role in cancer have been described. In the present review, based on the evidence of SIRT-3 involvement in metabolic dysfunctions, we aimed to provide an insight into the multifaceted role of SIRT-3 in many solid and hematological tumors with a particular focus on hepatocellular carcinoma (HCC)...
May 19, 2017: Digestive Diseases and Sciences
https://www.readbyqxmd.com/read/28526414/a-novel-sirt1-inhibitor-4bb-induces-apoptosis-in-hct116-human-colon-carcinoma-cells-partially-by-activating-p53
#4
Ananga Ghosh, Amrita Sengupta, Guru Pavan Kumar Seerapu, Ali Nakhi, E V Venkat Shivaji Ramarao, Navneet Bung, Gopalakrishnan Bulusu, Manojit Pal, Devyani Haldar
The NAD+-dependent protein deacetylase SIRT1 has emerged as an important target for epigenetic therapeutics of colon cancer as its increased expression is associated with cancer progression. Additionally, SIRT1 represses p53 function via deacetylation, promoting tumor growth. Therefore, inhibition of SIRT1 is of great therapeutic interest for the treatment of colon cancer. Here, we report discovery of a novel quinoxaline based small molecule inhibitor of human SIRT1, 4bb, investigated its effect on viability of colon cancer cells and molecular mechanism of action...
May 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28525376/exploiting-ros-and-metabolic-differences-to-kill-cisplatin-resistant-lung-cancer
#5
Medhi Wangpaichitr, Chunjing Wu, Ying Ying Li, Dan J M Nguyen, Hande Kandemir, Sumedh Shah, Shumei Chen, Lynn G Feun, Jeffrey S Prince, Macus T Kuo, Niramol Savaraj
Cisplatin resistance remains a major problem in the treatment of lung cancer. We have discovered that cisplatin resistant (CR) lung cancer cells, regardless of the signaling pathway status, share the common parameter which is an increase in reactive oxygen species (ROS) and undergo metabolic reprogramming. CR cells were no longer addicted to the glycolytic pathway, but rather relied on oxidative metabolism. They took up twice as much glutamine and were highly sensitive to glutamine deprivation. Glutamine is hydrolyzed to glutamate for glutathione synthesis, an essential factor to abrogate high ROS via xCT antiporter...
May 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28515364/nicotinamide-metabolism-regulates-glioblastoma-stem-cell-maintenance
#6
Jinkyu Jung, Leo J Y Kim, Xiuxing Wang, Qiulian Wu, Tanwarat Sanvoranart, Christopher G Hubert, Briana C Prager, Lisa C Wallace, Xun Jin, Stephen C Mack, Jeremy N Rich
Metabolic dysregulation promotes cancer growth through not only energy production, but also epigenetic reprogramming. Here, we report that a critical node in methyl donor metabolism, nicotinamide N-methyltransferase (NNMT), ranked among the most consistently overexpressed metabolism genes in glioblastoma relative to normal brain. NNMT was preferentially expressed by mesenchymal glioblastoma stem cells (GSCs). NNMT depletes S-adenosyl methionine (SAM), a methyl donor generated from methionine. GSCs contained lower levels of methionine, SAM, and nicotinamide, but they contained higher levels of oxidized nicotinamide adenine dinucleotide (NAD+) than differentiated tumor cells...
May 18, 2017: JCI Insight
https://www.readbyqxmd.com/read/28514875/identification-of-novel-nicotinamide-phosphoribosyltransferase-nampt-inhibitors-using-computational-approaches
#7
Manish Kesherwani, Sriram Raghavan, Krishnasamy Gunasekaran, Devadasan Velmurugan
Nicotinamide Phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the biosynthesis of NAD. Cancer cells have elevated poly [ADP-Ribose] polymerase 1 (PARP) activity as well as the immense necessity of ATP: thereby consuming NAD at a higher rate than normal tissues. The perturbation of these intracellular processes is more sensitive and highly dependent on NAMPT to maintain the required NAD levels. Functional inhibition of NAMPT is, therefore, a promising drug target in therapeutic oncology. In this study, the importance of intermolecular contacts was realized based on contact occupancy and favorable energetic from molecular dynamic simulation to discern non-critical contacts of four different classes of potential NAMPT inhibitor bound complexes...
May 17, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28507103/nicotinic-acid-phosphoribosyltransferase-regulates-cancer-cell-metabolism-susceptibility-to-nampt-inhibitors-and-dna-repair
#8
Francesco Piacente, Irene Caffa, Silvia Ravera, Giovanna Sociali, Mario Passalacqua, Valerio G Vellone, Pamela Becherini, Daniele Reverberi, Fiammetta Monacelli, Alberto Ballestrero, Patrizio Odetti, Antonia Cagnetta, Michele Cea, Aimable Nahimana, Michel A Duchosal, Santina Bruzzone, Alessio Nencioni
In the last decade, substantial efforts have been made to identify NAD+ biosynthesis inhibitors, specifically against nicotinamide phosphoribosyltransferase (NAMPT), as preclinical studies indicate their potential efficacy as cancer drugs. However, the clinical activity of NAMPT inhibitors has proven limited, suggesting that alternative NAD+ production routes exploited by tumors confer resistance. Here we show the gene encoding nicotinic acid phosphoribosyltransferase (NAPRT), a second NAD+ producing enzyme, is amplified and overexpressed in a subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a BRCAness gene expression signature...
May 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28503686/mesoporous-nanocarriers-with-a-stimulus-responsive-cyclodextrin-gatekeeper-for-targeting-tumor-hypoxia
#9
Jeonghun Lee, Eun-Taex Oh, Haerry Yoon, Chan Woo Kim, Yeji Han, Jaehun Song, Hyunil Jang, Heon Joo Park, Chulhee Kim
Tissue hypoxia developed in most malignant tumors makes a significant difference to normal tissues in the reduction potential and the activity of various bioreductive enzymes. Given the superior enzymatic activity of NAD(P)H:quinone oxidoreductase 1 (NQO1, a cytosolic reductase up-regulated in many human cancers) in hypoxia relative to that in normoxia, NQO1 has great potential for targeting hypoxic tumor cells. In the present report, the core concept of hypoxic NQO1-responsive mesoporous silica nanoparticles (MSNs) is based on the reasoning that the superior enzymatic activity of NQO1 within hypoxic cancer cells can be utilized as a key stimulus for the selective cleavage of an azobenzene stalk triggering the on-off gatekeeping for controlled release of guest drugs...
May 25, 2017: Nanoscale
https://www.readbyqxmd.com/read/28498397/dihydroartemisinin-inhibits-the-viability-of-cervical-cancer-cells-by-upregulating-caveolin%C3%A2-1-and-mitochondrial-carrier-homolog%C3%A2-2-involvement-of-p53-activation-and-nad-p-h-quinone-oxidoreductase%C3%A2-1-downregulation
#10
Ting Zhang, Yuan Hu, Ting Wang, Peiling Cai
Dihydroartemisinin (DHA) has been shown to inhibit the viability of various cancer cells. Previous studies have revealed that the mechanisms involved in the inhibitory effects of DHA are based on theactivation of p53 and the mitochondrial-related cell death pathway. However, the exact association between upstream signaling and the activation of cell death pathway remains unclear. In this study, we found that DHA treatment induced the upregulation of caveolin 1 (Cav1) and mitochondrial carrier homolog 2 (MTCH2) in HeLa cells, and this was associated with the DHA-induced inhibition of cell viability and DHA-induced apoptosis...
May 9, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28496053/chemical-and-structural-biology-of-protein-lysine-deacetylases
#11
Minoru Yoshida, Norio Kudo, Saori Kosono, Akihiro Ito
Histone acetylation is a reversible posttranslational modification that plays a fundamental role in regulating eukaryotic gene expression and chromatin structure/function. Key enzymes for removing acetyl groups from histones are metal (zinc)-dependent and NAD(+)-dependent histone deacetylases (HDACs). The molecular function of HDACs have been extensively characterized by various approaches including chemical, molecular, and structural biology, which demonstrated that HDACs regulate cell proliferation, differentiation, and metabolic homeostasis, and that their alterations are deeply involved in various human disorders including cancer...
2017: Proceedings of the Japan Academy. Series B, Physical and Biological Sciences
https://www.readbyqxmd.com/read/28488541/microrna-124-suppresses-proliferation-and-glycolysis-in-non-small-cell-lung-cancer-cells-by-targeting-akt-glut1-hkii
#12
Xiaojian Zhao, Caiping Lu, Weiwei Chu, Bing Zhang, Qiang Zhen, Renfeng Wang, Yaxiao Zhang, Zhe Li, Baolei Lv, Huixian Li, Jiabao Liu
Non-small cell lung cancer accounts for 85% of all types of lung cancer and is the leading cause of worldwide cancer-associated mortalities. MiR-124 is epigenetically silenced in various types of cancer and plays important roles in tumor development and progression. MiR-124 was also significantly downregulated in non-small cell lung cancer patients. Glycolysis has been considered as a feature of cancer cells; hypoxia-inducible factor 1-alpha/beta and Akt are key enzymes in the regulation of glycolysis and energy metabolism in cancer cells...
May 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28487966/oligomeric-proanthocyanidins-protects-a549-cells-against-h2o2-induced-oxidative-stress-via-the-nrf2-are-pathway
#13
Chao Sun, Weiguo Jin, Hongcan Shi
Oxidative signaling and oxidative stress contribute to aging, cancer and diseases resulting from lung fibrosis. In this study, we explored the anti-oxidative potential of oligomeric proanthocyanidins (OPCs), natural flavonoid compounds. We examined the protective effects of OPCs against hydrogen peroxide (H2O2)-induced oxidative stress in non-small cell lung cancer cells (A549). We demonstrated that OPC markedly attenuated H2O2-induced A549 cell viability, as shown by by 3-[4,5-dimethylthiazol-2-yl)]-2,5-diphenyl-tetrazolium bromide (MTT) assay...
June 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28485124/autofluorescence-imaging-identifies-tumor-cell-cycle-status-on-a-single-cell-level
#14
Tiffany M Heaster, Alex J Walsh, Yue Zhao, Scott W Hiebert, Melissa C Skala
The goal of this study is to validate fluorescence intensity and lifetime imaging of metabolic co-enzymes NAD(P)H and FAD (optical metabolic imaging, or OMI) as a method to quantify cell-cycle status of tumor cells. Heterogeneity in tumor cell-cycle status (e. g. proliferation, quiescence, apoptosis) increases drug resistance and tumor recurrence. Cell-cycle status is closely linked to cellular metabolism. Thus, this study applies cell-level metabolic imaging to distinguish proliferating, quiescent, and apoptotic populations...
May 9, 2017: Journal of Biophotonics
https://www.readbyqxmd.com/read/28482792/poly-adp-ribosyl-polymerase-1-inhibitors-a-patent-review
#15
Mengda Cao, Xi Sun, Yanjun Zhou, Wen Huang, Ling Meng, Ji-Fu Wei
BACKGROUND: Poly (ADP-ribosyl) polymerase 1 (PARP1) is important in maintaining genomic stability, repairing DNA damage, and regulating transcriptional processes. Altered PARP1 activity is associated with a multitude of pathologies especially cancer. The broad application prospects of PARP1 inhibitors attract many well-known pharmaceutical companies, which promotes the development of PARP1 inhibitors. Objective:Present review aims to introduce PARP1 inhibitors by their structures and try to point out future development direction of PARP1 inhibitors...
May 8, 2017: Recent Patents on Anti-cancer Drug Discovery
https://www.readbyqxmd.com/read/28476035/rewiring-carbohydrate-catabolism-differentially-affects-survival-of-pancreatic-cancer-cell-lines-with-diverse-metabolic-profiles
#16
Tiziana Tataranni, Francesca Agriesti, Vitalba Ruggieri, Carmela Mazzoccoli, Vittorio Simeon, Ilaria Laurenzana, Rosella Scrima, Valerio Pazienza, Nazzareno Capitanio, Claudia Piccoli
An increasing body of evidence suggests that targeting cellular metabolism represents a promising effective approach to treat pancreatic cancer, overcome chemoresistance and ameliorate patient's prognosis and survival. In this study, following whole-genome expression analysis, we selected two pancreatic cancer cell lines, PANC-1 and BXPC-3, hallmarked by distinct metabolic profiles with specific concern to carbohydrate metabolism. Functional comparative analysis showed that BXPC-3 displayed a marked deficit of the mitochondrial respiratory and oxidative phosphorylation activity and a higher production of reactive oxygen species and a reduced NAD+/NADH ratio, indicating their bioenergetic reliance on glycolysis and a different redox homeostasis as compared to PANC-1...
April 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/28468779/discovery-and-characterization-of-novel-non-substrate-and-substrate-nampt-inhibitors
#17
Julie L Wilsbacher, Min Cheng, Dong Cheng, Samuel A J Trammell, Yan Shi, Jun Guo, Stormy L Koeniger, Peter J Kovar, Yupeng He, Sujatha Selvaraju, H Robin Heyman, Bryan K Sorensen, Richard F Clark, T Matthew Hansen, Kenton L Longenecker, Diana Raich, Alla V Korepanova, Steven Cepa, Danli L Towne, Vivek C Abraham, Hua Tang, Paul L Richardson, Shaun M McLoughlin, Ilaria Badagnani, Michael L Curtin, Michael R Michaelides, David Maag, F Greg Buchanan, Gary G Chiang, Wenqing Gao, Saul H Rosenberg, Charles Brenner, Chris Tse
Cancer cells are highly reliant on nicotinamide adenine dinucleotide (NAD(+))-dependent processes including glucose metabolism, calcium signaling, DNA repair, and regulation of gene expression. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) salvage from nicotinamide (NAM), has been investigated as a target for anti-cancer therapy. Known NAMPT inhibitors with potent cell activity are composed of a nitrogen-containing aromatic group, which is phosphoribosylated by the enzyme...
May 3, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28468736/prevention-of-non-melanoma-skin-cancers-with-nicotinamide-in-transplant-recipients-a-case-control-study
#18
Francesco Drago, Giulia Ciccarese, Ludovica Cogorno, Camillo Calvi, Luigina A Marsano, Aurora Parodi
Nicotinamide is the precursor of nicotinamide adenine dinucleotide (NAD+), an essential cofactor for adenosine triphosphate (ATP) production. It has recently been reported to be effective in reducing the rates of new non-melanoma skin cancers (NMSCs) and actinic keratosis (AKs). We studied the efficacy of oral nicotinamide as treatment for AKs in transplant recipients. We recruited 38 transplant (eight liver and 30 kidney) patients with single or multiple AKs. Nineteen patients were randomly assigned to Group 1 and took nicotinamide 500 mg/daily (cases); the other 19 patients were randomly assigned to Group 2 without nicotinamide (controls)...
May 3, 2017: European Journal of Dermatology: EJD
https://www.readbyqxmd.com/read/28455582/glutathione-s-transferases-deletions-may-act-as-prognosis-and-therapeutic-markers-in-breast-cancer
#19
Clodoaldo Zago Campos, Roberta Losi Guembarovski, Carlos Eduardo Coral de Oliveira, Bruna Karina Banin Hirata, Glauco Akelinghton Freire Vitiello, Flávia Luísa Dias, Carlos Hiroji Hiroki, Maria Angelica Ehara Watanabe, Tânia Longo Mazzuco
Breast cancer (BC) is the main worldwide neoplasia in women. The metabolic balance between xenobiotic absorption and elimination rates plays an important role in preventing DNA damage and, consequently, tumor development. The glutathione S-transferases (GSTs), such as GSTM1 and GSTT1, and the NAD(P)H quinone oxidoreductase are important enzymes involved in phase II detoxification reactions. Deletions in GSTM1 and GSTT1, and single-nucleotide polymorphism (SNP) in NQO1 (rs1800655) have been investigated in cancer context, revealing conflicting results...
April 28, 2017: Clinical and Experimental Medicine
https://www.readbyqxmd.com/read/28435470/downregulation-of-sirt7-by-5-fluorouracil-induces-radiosensitivity-in-human-colorectal-cancer
#20
Ming Tang, Xiaopeng Lu, Chaohua Zhang, Changzheng Du, Linlin Cao, Tianyun Hou, Zhiming Li, Bo Tu, Ziyang Cao, Yinglu Li, Yongcan Chen, Lu Jiang, Hui Wang, Lina Wang, Baohua Liu, Xingzhi Xu, Jianyuan Luo, Jiadong Wang, Jin Gu, Haiying Wang, Wei-Guo Zhu
5-Fluorouracil (5-FU) combined with radiotherapy is a common treatment strategy to treat human cancers, but the underlying mechanisms of this combination treatment remain unclear. Here, we report that NAD(+)-dependent deacetylase sirtuin-7 (SIRT7) protein levels were decreased due to 5-FU exposure rendering colorectal cancer cells sensitive to radiation. We found that SIRT7 downregulation was mediated via a Tat-binding Protein 1 (TBP1) proteasome-dependent pathway. Specifically, TBP1 was dephosphorylated at tyrosine 381 upon 5-FU treatment, which enhanced its direct interaction with SIRT7 and targeted it for degradation...
2017: Theranostics
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