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https://www.readbyqxmd.com/read/28061878/blockage-of-glycolysis-by-targeting-pfkfb3-suppresses-tumor-growth-and-metastasis-in-head-and-neck-squamous-cell-carcinoma
#1
Hui-Min Li, Jie-Gang Yang, Zhuo-Jue Liu, Wei-Ming Wang, Zi-Li Yu, Jian-Gang Ren, Gang Chen, Wei Zhang, Jun Jia
BACKGROUND: Many cancers including head and neck squamous cell carcinoma (HNSCC) are characterized by a metabolic rewiring with increased glucose uptake and lactate production, termed as aerobic glycolysis. Targeting aerobic glycolysis presents a promising strategy for cancer therapy. This study investigates the therapeutic potential of glycolysis blockage by targeting phosphofructokinase-2/fructose-2, 6-bisphosphatase 3 (PFKFB3) in HNSCC. METHODS: 1-(4-pyridinyl)-3-(2-quinolinyl)-2-propen-1-one (PFK15) was used as a selective antagonist of PFKFB3...
January 7, 2017: Journal of Experimental & Clinical Cancer Research: CR
https://www.readbyqxmd.com/read/28049552/antiproliferative-cyclodepsipeptides-from-the-marine-actinomycete-streptomyces-sp-p11-23b-downregulating-the-tumor-metabolic-enzymes-of-glycolysis-glutaminolysis-and-lipogenesis
#2
Xuewei Ye, Komal Anjum, Tengfei Song, Wenling Wang, Ying Liang, Mengxuan Chen, Haocai Huang, Xiao-Yuan Lian, Zhizhen Zhang
Two cyclodepsipeptides and a known cyclodepsipeptide valinomycin were isolated from a culture of the marine actinomycete Streptomyces sp. P11-23B. Their structures were established based on NMR, HRESIMS, and MS-MS spectroscopic interpretation as well as by chemical degradation. Both streptodepsipeptides P11A and P11B inhibited proliferation of different glioma cell lines, with IC50 values ranging from 0.1 μM to 1.4 μM. Streptodepsipeptide P11A was found to block the cell cycle at the G0/G1 phase and induce apoptosis in glioma cells...
December 31, 2016: Phytochemistry
https://www.readbyqxmd.com/read/27983531/pfkfb3-was-overexpressed-in-gastric-cancer-patients-and-promoted-the-proliferation-and-migration-of-gastric-cancer-cells
#3
Jun Han, Qingyang Meng, Qiulei Xi, Haiyu Wang, Guohao Wu
OBJECTIVE: Gastric cancer is one of the most common cancers worldwide, and the prognosis is still very poor due to the lack of specific and sensitive biomarkers. Aerobic glycolysis is one of the critical hallmarks of gastric cancer cells, and several glycolytic enzymes are highly expressed in gastric cancer patients. However, the expression and clinical significances of phosphofructokinase-2/fructose-2,6-bisphosphatase3 (PFKFB3, one of the glycolytic enzymes) in a large sample of gastric cancer patients remain unclear...
December 9, 2016: Cancer Biomarkers: Section A of Disease Markers
https://www.readbyqxmd.com/read/27960081/to-pfkfb3-or-not-to-pfkfb3-that-is-the-question
#4
Cristina Branco, Randall S Johnson
In this issue of Cancer Cell, Cantelmo et al. describe how reduction of PFKFB3 enzyme activity can promote vascular normalization. The authors show in turn how this affects vascular permeability and can ultimately improve the efficacy of chemotherapeutic agents.
December 12, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27922662/metabolic-reprogramming-and-ampk%C3%AE-1-pathway-activation-by-caulerpin-in-colorectal-cancer-cells
#5
Hua Yu, Huiqin Zhang, Mingjun Dong, Zhou Wu, Zhonglei Shen, Yangyang Xie, Zhenfang Kong, Xiaoyu Dai, Binbin Xu
Caulerpin, a secondary metabolite from the marine invasive green algae Caulerpa cylindracea is known to induce mitochondrial dysfunctions. In this study, the anticancer property of caulerpin was assessed in a panel of colorectal cancer cell lines. We demonstrated that caulerpin inhibited oxidative phosphorylation (OXPHOS) and facilitated an early intervention of the mitochondrial function, via inhibiting mitochondrial complex I, accompanied by the dissipation of mitochondrial membrane potential and a surge of reactive oxygen species (ROS) generation...
January 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/27901115/p53-coordinates-dna-repair-with-nucleotide-synthesis-by-suppressing-pfkfb3-expression-and-promoting-the-pentose-phosphate-pathway
#6
Derek A Franklin, Yizhou He, Patrick L Leslie, Andrey P Tikunov, Nick Fenger, Jeffrey M Macdonald, Yanping Zhang
Activation of p53 in response to DNA damage is essential for tumor suppression. Although previous studies have emphasized the importance of p53-dependent cell cycle arrest and apoptosis for tumor suppression, recent studies have suggested that other areas of p53 regulation, such as metabolism and DNA damage repair (DDR), are also essential for p53-dependent tumor suppression. However, the intrinsic connections between p53-mediated DDR and metabolic regulation remain incompletely understood. Here, we present data suggesting that p53 promotes nucleotide biosynthesis in response to DNA damage by repressing the expression of the phosphofructokinase-2 (PFK2) isoform 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a rate-limiting enzyme that promotes glycolysis...
November 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27884166/tigar-cooperated-with-glycolysis-to-inhibit-the-apoptosis-of-leukemia-cells-and-associated-with-poor-prognosis-in-patients-with-cytogenetically-normal-acute-myeloid-leukemia
#7
Sixuan Qian, Jianyong Li, Ming Hong, Yu Zhu, Huihui Zhao, Yue Xie, Jiayu Huang, Yun Lian, Yanru Li, Shuai Wang, Jianping Mao, Yaoyu Chen
BACKGROUND: Cancer cells show increased glycolysis and take advantage of this metabolic pathway to generate ATP. The TP53-induced glycolysis and apoptosis regulator (TIGAR) inhibits aerobic glycolysis and protects tumor cells from intracellular reactive oxygen species (ROS)-associated apoptosis. However, the function of TIGAR in glycolysis and survival of acute myeloid leukemia cells remains unclear. METHODS: We analyzed TIGAR expression in cytogenetically normal (CN-) AML patients and the correlations with clinical and biological parameters...
November 25, 2016: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/27866851/inhibition-of-the-glycolytic-activator-pfkfb3-in-endothelium-induces-tumor-vessel-normalization-impairs-metastasis-and-improves-chemotherapy
#8
Anna Rita Cantelmo, Lena-Christin Conradi, Aleksandra Brajic, Jermaine Goveia, Joanna Kalucka, Andreas Pircher, Pallavi Chaturvedi, Johanna Hol, Bernard Thienpont, Laure-Anne Teuwen, Sandra Schoors, Bram Boeckx, Joris Vriens, Anna Kuchnio, Koen Veys, Bert Cruys, Lise Finotto, Lucas Treps, Tor Espen Stav-Noraas, Francesco Bifari, Peter Stapor, Ilaria Decimo, Kim Kampen, Katrien De Bock, Guttorm Haraldsen, Luc Schoonjans, Ton Rabelink, Guy Eelen, Bart Ghesquière, Jalees Rehman, Diether Lambrechts, Asrar B Malik, Mieke Dewerchin, Peter Carmeliet
Abnormal tumor vessels promote metastasis and impair chemotherapy. Hence, tumor vessel normalization (TVN) is emerging as an anti-cancer treatment. Here, we show that tumor endothelial cells (ECs) have a hyper-glycolytic metabolism, shunting intermediates to nucleotide synthesis. EC haplo-deficiency or blockade of the glycolytic activator PFKFB3 did not affect tumor growth, but reduced cancer cell invasion, intravasation, and metastasis by normalizing tumor vessels, which improved vessel maturation and perfusion...
December 12, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27803158/tp53-inducible-glycolysis-and-apoptosis-regulator-tigar-metabolically-reprograms-carcinoma-and-stromal-cells-in-breast-cancer
#9
Ying-Hui Ko, Marina Domingo-Vidal, Megan Roche, Zhao Lin, Diana Whitaker-Menezes, Erin Seifert, Claudia Capparelli, Madalina Tuluc, Ruth C Birbe, Patrick Tassone, Joseph M Curry, Àurea Navarro-Sabaté, Anna Manzano, Ramon Bartrons, Jaime Caro, Ubaldo Martinez-Outschoorn
A subgroup of breast cancers has several metabolic compartments. The mechanisms by which metabolic compartmentalization develop in tumors are poorly characterized. TP53 inducible glycolysis and apoptosis regulator (TIGAR) is a bisphosphatase that reduces glycolysis and is highly expressed in carcinoma cells in the majority of human breast cancers. Hence we set out to determine the effects of TIGAR expression on breast carcinoma and fibroblast glycolytic phenotype and tumor growth. The overexpression of this bisphosphatase in carcinoma cells induces expression of enzymes and transporters involved in the catabolism of lactate and glutamine...
December 16, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27777982/a-molecular-signature-of-preclinical-rheumatoid-arthritis-triggered-by-dysregulated-ptpn22
#10
Hui-Hsin Chang, Guang-Yaw Liu, Nishant Dwivedi, Bo Sun, Yuko Okamoto, Jennifer D Kinslow, Kevin D Deane, M Kristen Demoruelle, Jill M Norris, Paul R Thompson, Jeffrey A Sparks, Deepak A Rao, Elizabeth W Karlson, Hui-Chih Hung, V Michael Holers, I-Cheng Ho
A unique feature of rheumatoid arthritis (RA) is the presence of anti-citrullinated protein antibodies (ACPA). Several risk factors for RA are known to increase the expression or activity of peptidyl arginine deiminases (PADs), which catalyze citrullination and, when dysregulated, can result in hypercitrullination. However, the consequence of hypercitrullination is unknown and the function of each PAD has yet to be defined. Th cells of RA patients are hypoglycolytic and hyperproliferative due to impaired expression of PFKFB3 and ATM, respectively...
October 20, 2016: JCI Insight
https://www.readbyqxmd.com/read/27682256/impact-of-heat-stress-on-cellular-and-transcriptional-adaptation-of-mammary-epithelial-cells-in-riverine-buffalo-bubalus-bubalis
#11
Neha Kapila, Ankita Sharma, Amit Kishore, Monika Sodhi, Pawan K Tripathi, Ashok K Mohanty, Manishi Mukesh
The present study aims to identify the heat responsive genes and biological pathways in heat stressed buffalo mammary epithelial cells (MECs). The primary mammary epithelial cells of riverine buffalo were exposed to thermal stress at 42°C for one hour. The cells were subsequently allowed to recover at 37°C and harvested at different time intervals (30 min to 48 h) along with control samples (un-stressed). In order to assess the impact of heat stress in buffalo MECs, several in-vitro cellular parameters (lactate dehydrogenase activity, cell proliferation assay, cellular viability, cell death and apoptosis) and transcriptional studies were conducted...
2016: PloS One
https://www.readbyqxmd.com/read/27669567/pfk15-a-small-molecule-inhibitor-of-pfkfb3-induces-cell-cycle-arrest-apoptosis-and-inhibits-invasion-in-gastric-cancer
#12
Wei Zhu, Liang Ye, Jianzhao Zhang, Pengfei Yu, Hongbo Wang, Zuguang Ye, Jingwei Tian
PFKFB3 (6-phosphofructo-2-kinase) synthesizes fructose 2,6-bisphosphate (F2,6P2), which is an allosteric activator of 6-phosphofructo-1-kinase (PFK-1), the rate-limiting enzyme of glycolysis. Overexpression of the PFKFB3 enzyme leads to high glycolytic metabolism, which is required for cancer cells to survive in the harsh tumor microenvironment. The objective of this study was to investigate the antitumor activity of PFK15 (1-(4-pyridinyl)-3-(2-quinolinyl)-2-propen-1-one), a small molecule inhibitor of PFKFB3, against gastric cancer and to explore its potential mechanisms...
2016: PloS One
https://www.readbyqxmd.com/read/27613609/inhibition-of-6-phosphofructo-2-kinase-pfkfb3-suppresses-glucose-metabolism-and-the-growth-of-her2-breast-cancer
#13
Julie O'Neal, Amy Clem, Lindsey Reynolds, Susan Dougherty, Yoannis Imbert-Fernandez, Sucheta Telang, Jason Chesney, Brian F Clem
PURPOSE: Human epidermal growth factor receptor-2 (HER2) has been implicated in the progression of multiple tumor types, including breast cancer, and many downstream effectors of HER2 signaling are primary regulators of cellular metabolism, including Ras and Akt. A key downstream metabolic target of Ras and Akt is the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 isozyme (PFKFB3), whose product, fructose-2,6-bisphosphate (F26BP), is a potent allosteric activator of a rate-limiting enzyme in glycolysis, 6-phosphofructo-1-kinase (PFK-1)...
November 2016: Breast Cancer Research and Treatment
https://www.readbyqxmd.com/read/27585591/ikk%C3%AE-promotes-metabolic-adaptation-to-glutamine-deprivation-via-phosphorylation-and-inhibition-of-pfkfb3
#14
Michael A Reid, Xazmin H Lowman, Min Pan, Thai Q Tran, Marc O Warmoes, Mari B Ishak Gabra, Ying Yang, Jason W Locasale, Mei Kong
Glutamine is an essential nutrient for cancer cell survival and proliferation. Enhanced utilization of glutamine often depletes its local supply, yet how cancer cells adapt to low glutamine conditions is largely unknown. Here, we report that IκB kinase β (IKKβ) is activated upon glutamine deprivation and is required for cell survival independently of NF-κB transcription. We demonstrate that IKKβ directly interacts with and phosphorylates 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase isoform 3 (PFKFB3), a major driver of aerobic glycolysis, at Ser269 upon glutamine deprivation to inhibit its activity, thereby down-regulating aerobic glycolysis when glutamine levels are low...
August 15, 2016: Genes & Development
https://www.readbyqxmd.com/read/27566823/pfkfb3-driven-macrophage-glycolytic-metabolism-is-a-crucial-component-of-innate-antiviral-defense
#15
Hui Jiang, Hengfei Shi, Man Sun, Yafeng Wang, Qingzhou Meng, Panpan Guo, Yanlan Cao, Jiong Chen, Xiang Gao, Erguang Li, Jianghuai Liu
Signaling by viral nucleic acids and subsequently by type I IFN is central to antiviral innate immunity. These signaling events are also likely to engage metabolic changes in immune and nonimmune cells to support antiviral defense. In this study, we show that cytosolic viral recognition, by way of secondary IFN signaling, leads to upregulation of glycolysis preferentially in macrophages. This metabolic switch involves induction of glycolytic activator 6-phosphofructose-2-kinase and fructose-2,6-bisphosphatase (PFKFB3)...
October 1, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27535281/the-epigenetic-signature-of-systemic-insulin-resistance-in-obese-women
#16
Peter Arner, Anna-Stina Sahlqvist, Indranil Sinha, Huan Xu, Xiang Yao, Dawn Waterworth, Deepak Rajpal, A Katrina Loomis, Johannes M Freudenberg, Toby Johnson, Anders Thorell, Erik Näslund, Mikael Ryden, Ingrid Dahlman
AIMS/HYPOTHESIS: Insulin resistance (IR) links obesity to type 2 diabetes. The aim of this study was to explore whether white adipose tissue (WAT) epigenetic dysregulation is associated with systemic IR by genome-wide CG dinucleotide (CpG) methylation and gene expression profiling in WAT from insulin-resistant and insulin-sensitive women. A secondary aim was to determine whether the DNA methylation signature in peripheral blood mononuclear cells (PBMCs) reflects WAT methylation and, if so, can be used as a marker for systemic IR...
November 2016: Diabetologia
https://www.readbyqxmd.com/read/27491149/-expression-of-pfkfb-hk2-nampt-tspan13-and-hspb8-genes-in-pediatric-glioma
#17
D O Minchenko, Y E Novik, H S Maslak, O V Tiazhka, O H Minchenko
We studied the peculiarity of the expression of several key genes related to dysregulation of cell proliferation and surviving processes in pediatric glioma (glioblastoma multiforme) tissue from five children with age from 5 to 8 years as well a sin corresponding nonmalignant tissue counterparts as control from the same patients. RNA was isolated from glioma tissue and corresponding non-malignant tissue counterparts and PFKFB1, PFKFB2, PFKFB3, PFKFB4, HK2, NAMPT, TSPAN13, and HSPB8 gene expressions were studied by quantitative polymerase chain reaction...
October 2015: Likars'ka Sprava
https://www.readbyqxmd.com/read/27436424/glycolytic-regulation-of-cell-rearrangement-in-angiogenesis
#18
Bert Cruys, Brian W Wong, Anna Kuchnio, Dries Verdegem, Anna Rita Cantelmo, Lena-Christin Conradi, Saar Vandekeere, Ann Bouché, Ivo Cornelissen, Stefan Vinckier, Roeland M H Merks, Elisabetta Dejana, Holger Gerhardt, Mieke Dewerchin, Katie Bentley, Peter Carmeliet
During vessel sprouting, endothelial cells (ECs) dynamically rearrange positions in the sprout to compete for the tip position. We recently identified a key role for the glycolytic activator PFKFB3 in vessel sprouting by regulating cytoskeleton remodelling, migration and tip cell competitiveness. It is, however, unknown how glycolysis regulates EC rearrangement during vessel sprouting. Here we report that computational simulations, validated by experimentation, predict that glycolytic production of ATP drives EC rearrangement by promoting filopodia formation and reducing intercellular adhesion...
2016: Nature Communications
https://www.readbyqxmd.com/read/27387960/glucose-and-palmitate-differentially-regulate-pfkfb3-ipfk2-and-inflammatory-responses-in-mouse-intestinal-epithelial-cells
#19
Rachel Botchlett, Honggui Li, Xin Guo, Ting Qi, JiaJia Zhao, Juan Zheng, Shih-Lung Woo, Ya Pei, Mengyang Liu, Xiang Hu, Guang Chen, Ting Guo, Sijun Yang, Qifu Li, Xiaoqiu Xiao, Yuqing Huo, Chaodong Wu
The gene PFKFB3 encodes for inducible 6-phosphofructo-2-kinase, a glycolysis-regulatory enzyme that protects against diet-induced intestine inflammation. However, it is unclear how nutrient overload regulates PFKFB3 expression and inflammatory responses in intestinal epithelial cells (IECs). In the present study, primary IECs were isolated from small intestine of C57BL/6J mice fed a low-fat diet (LFD) or high-fat diet (HFD) for 12 weeks. Additionally, CMT-93 cells, a cell line for IECs, were cultured in low glucose (LG, 5...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27373212/targeting-of-mct1-and-pfkfb3-influences-cell-proliferation-and-apoptosis-in-bladder-cancer-by-altering-the-tumor-microenvironment
#20
Ke Yao Hu, De Gui Wang, Peng Fei Liu, Yan Wei Cao, Yong Hua Wang, Xue Cheng Yang, Cheng Xia Hu, Li Jiang Sun, Hai Tao Niu
Phosphofructokinase-2/fructose-2,6-bisphosphatase 3 (PFKFB3) and monocarboxylate transporter 1 (MCT1) play important roles in tumor endothelial cells (ECs) and several biological processes. The present study was conducted to study the effects of PFKFB3 and MCT1 on cell proliferation and apoptosis in the tumor microenvironment by co-culture of HUVECs and T24, a bladder cancer (BC) cell line, using a microfluidic device. Immunofluorescence assay showed that HUVEC activity was significantly enhanced under co-culture with T24 cells, according to the stronger fluorescence intensity of CD31 and CD105 than that in the signal‑cultured cells...
August 2016: Oncology Reports
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