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https://www.readbyqxmd.com/read/28316886/identification-of-dysregulated-genes-in-rheumatoid-arthritis-based-on-bioinformatics-analysis
#1
Ruihu Hao, Haiwei Du, Lin Guo, Fengde Tian, Ning An, Tiejun Yang, Changcheng Wang, Bo Wang, Zihao Zhou
BACKGROUND: Rheumatoid arthritis (RA) is a chronic auto-inflammatory disorder of joints. The present study aimed to identify the key genes in RA for better understanding the underlying mechanisms of RA. METHODS: The integrated analysis of expression profiling was conducted to identify differentially expressed genes (DEGs) in RA. Moreover, functional annotation, protein-protein interaction (PPI) network and transcription factor (TF) regulatory network construction were applied for exploring the potential biological roles of DEGs in RA...
2017: PeerJ
https://www.readbyqxmd.com/read/28239846/inhibition-of-6-phosphofructo-2-kinase-suppresses-fibroblast-like-synoviocytes-mediated-synovial-inflammation-and-joint-destruction-in-rheumatoid-arthritis
#2
Yaoyao Zou, Shan Zeng, Mingcheng Huang, Qian Qiu, Youjun Xiao, Maohua Shi, Zhongping Zhan, Liuqin Liang, Xiuyan Yang, Hanshi Xu
BACKGROUND AND PURPOSE: Abnormal glycolytic metabolism contributes to joint inflammation in rheumatoid arthritis (RA). The aims of this study were to investigate the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a bifunctional enzyme that controls the glycolytic rate, in regulating fibroblast-like synoviocyte (FLS)-mediated synovial inflammation and invasiveness in RA. EXPERIMENTAL APPROACH: A specific PFKFB3 inhibitor, PFK15, and siRNA were used to evaluate the role of PFKFB3...
February 27, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28235572/role-of-akt-pkb-and-pfkfb-isoenzymes-in-the-control-of-glycolysis-cell-proliferation-and-protein-synthesis-in-mitogen-stimulated-thymocytes
#3
Amina Houddane, Laurent Bultot, Laura Novellasdemunt, Manuel Johanns, Marie-Agnès Gueuning, Didier Vertommen, Pierre G Coulie, Ramon Bartrons, Louis Hue, Mark H Rider
Proliferating cells depend on glycolysis mainly to supply precursors for macromolecular synthesis. Fructose 2,6-bisphosphate (Fru-2,6-P2) is the most potent positive allosteric effector of 6-phosphofructo-1-kinase (PFK-1), and hence of glycolysis. Mitogen stimulation of rat thymocytes with concanavalin A (ConA) led to time-dependent increases in lactate accumulation (6-fold), Fru-2,6-P2 content (4-fold), 6-phosphofructo-2-kinase (PFK-2)/fructose-2,6-bisphosphatase isoenzyme 3 and 4 (PFKFB3 and PFKFB4) protein levels (~2-fold and ~15-fold, respectively) and rates of cell proliferation (~40-fold) and protein synthesis (10-fold) after 68h of incubation compared with resting cells...
February 22, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28212191/endothelial-cell-metabolism-an-update-anno-2017
#4
Laure-Anne Teuwen, Nihed Draoui, Charlotte Dubois, Peter Carmeliet
PURPOSE OF REVIEW: Endothelial cell metabolism has recently emerged as an important coregulator of angiogenesis and is therefore a promising new target in various angiogenesis-associated illnesses, like cancer. In this review, we discuss recent insights in endothelial cell metabolism in both physiological and pathological conditions and discuss possible translational implications. RECENT FINDINGS: Two metabolic pathways that determine the performance of endothelial cells are glycolysis and fatty acid oxidation (FAO)...
February 15, 2017: Current Opinion in Hematology
https://www.readbyqxmd.com/read/28173976/targeting-pfkfb3-in-the-endothelium-for-cancer-therapy
#5
Qi Yang, Peng Hou
In a recent article published in Cancer Cell, Cantelmo et al. showed that inhibition of endothelium glycolysis by targeting 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) significantly impaired tumor metastasis by normalizing tumor vessels. In addition, as a promising therapeutic strategy, tumor vessel normalization by PFKFB3 blockade also improved the delivery and efficacy of chemotherapy.
March 2017: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/28161638/6-phosphofructo-2-kinase-fructose-2-6-bisphosphatase-3-is-required-for-transforming-growth-factor-%C3%AE-1-enhanced-invasion-of-panc1-cells-in%C3%A2-vitro
#6
Abdullah Yalcin, Tugba H Solakoglu, Selahattin C Ozcan, Saime Guzel, Sabire Peker, Serap Celikler, Basak D Balaban, Elif Sevinc, Yunus Gurpinar, Jason A Chesney
Transforming growth factor β1 (TGFβ1) is a well-established inducer of the epithelial-mesenchymal transition (EMT) that is essential for the acquisition of malignant properties, such as invasion, in tumor cells. Although recent studies suggest that the EMT in tumor cells is associated with reprogramming of energy metabolism and TGFβ1 has been shown to stimulate glycolysis in multiple primary cell lines, little is known about TGFβ1's effect on glycolysis and glycolytic regulators in transformed cells. Given the known regulatory role of 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase-3 (PFKFB3) in glycolysis and association of glycolytic activity with malignant features such as invasion, we sought to investigate whether TGFβ1 regulates PFKFB3 expression and if PFKFB3 is involved in the TGFβ1-mediated increase in the invasive ability of the Panc1 cell cline-a well-established model of TGFβ1-initiated EMT...
March 11, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28152500/loss-of-pfkfb4-induces-cell-death-in-mitotically-arrested-ovarian-cancer-cells
#7
Charlotte Taylor, David Mannion, Fabrizio Miranda, Mohammad Karaminejadranjbar, Sandra Herrero-Gonzalez, Karin Hellner, Yiyan Zheng, Geoffrey Bartholomeusz, Robert C Bast, Ahmed Ashour Ahmed
Taxanes represent some of the most commonly used chemotherapeutic agents for ovarian cancer treatment. However, they are only effective in approximately 40% of patients. Novel therapeutic strategies are required to potentiate their effect and improve patient outcome. A hallmark of many cancers is the constitutive activation of the PI3K/AKT pathway, which drives cell survival and metabolism. We discovered a striking decrease in AKT activity coupled with a significant reduction in glucose 6-phosphate and ATP levels during mitotic arrest in the majority of ovarian cancer cell lines tested, indicating a potential metabolic vulnerability...
January 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/28108301/pfkfb3-a-direct-target-of-p63-is-required-for-proliferation-and-inhibits-differentiation-in-epidermal-keratinocytes
#8
Robert B Hamanaka, Gökhan M Mutlu
p63 is a transcription factor essential for epidermal development and homeostasis. p63 is a member of the p53 family of transcription factors, which are increasingly understood to be regulators of cellular metabolism. How p63 regulates metabolism in epidermal keratinocytes is incompletely understood, and it is unknown whether glycolytic regulation is essential to maintain the balance between proliferation and differentiation within the epidermis. We found that p63 promotes glycolytic metabolism in epidermal keratinocytes...
January 17, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28061878/blockage-of-glycolysis-by-targeting-pfkfb3-suppresses-tumor-growth-and-metastasis-in-head-and-neck-squamous-cell-carcinoma
#9
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
#10
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...
March 2017: Phytochemistry
https://www.readbyqxmd.com/read/27983531/pfkfb3-was-overexpressed-in-gastric-cancer-patients-and-promoted-the-proliferation-and-migration-of-gastric-cancer-cells
#11
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
#12
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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
#20
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
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