Excess glucose induces hypoxia-inducible factor-1α in pancreatic cancer cells and stimulates glucose metabolism and cell migration - Wikidata - awgldk - TriplyDB

Excess glucose induces hypoxia-inducible factor-1α in pancreatic cancer cells and stimulates glucose metabolism and cell migration

Excess glucose induces hypoxia-inducible factor-1α in pancreatic cancer cells and stimulates glucose metabolism and cell migration

http://www.wikidata.org/entity/Q39200208

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Mechanisms of regulation of PFKFB expression in pancreatic and gastric cancer cells Metabolic shifts toward glutamine regulate tumor growth, invasion and bioenergetics in ovarian cancer HIF-1α induces VE-cadherin expression and modulates vasculogenic mimicry in esophageal carcinoma cells.Impact of high glucose on metastasis of colon cancer cells Metformin inhibits gastric cancer via the inhibition of HIF1α/PKM2 signaling Insulin and hypoxia-inducible factor-1 cooperate in pancreatic cancer cells to increase cell viability Hypoxic resistance of KRAS mutant tumor cells to 3-Bromopyruvate is counteracted by Prima-1 and reversed by N-acetylcysteine.Association between metformin and the risk of gastric cancer in patients with type 2 diabetes mellitus: a meta-analysis of cohort studies.HIF-2α promotes epithelial-mesenchymal transition through regulating Twist2 binding to the promoter of E-cadherin in pancreatic cancer.Metabolism addiction in pancreatic cancer.Hexokinase 2 enhances the metastatic potential of tongue squamous cell carcinoma via the SOD2-H2O2 pathway.Glucose metabolic phenotype of pancreatic cancer.Metformin in pancreatic cancer treatment: from clinical trials through basic research to biomarker quantification.High glucose enhances the metastatic potential of tongue squamous cell carcinoma via the PKM2 pathway.Oscillating glucose and constant high glucose induce endoglin expression in endothelial cells: the role of oxidative stress.Emodin Decreases Hepatic Hypoxia-Inducible Factor-1[Formula: see text] by Inhibiting its Biosynthesis.Metabolic Features of Multiple Myeloma.

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Excess glucose induces hypoxia-inducible factor-1α in pancreatic cancer cells and stimulates glucose metabolism and cell migration

http://www.wikidata.org/entity/Q39200208

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年论文

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2013年论文

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name

Excess glucose induces hypoxia ...... metabolism and cell migration

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Excess glucose induces hypoxia ...... metabolism and cell migration.

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Excess glucose induces hypoxia ...... metabolism and cell migration

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Excess glucose induces hypoxia ...... metabolism and cell migration.

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Excess glucose induces hypoxia ...... metabolism and cell migration

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Excess glucose induces hypoxia ...... metabolism and cell migration.

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Cancer Biology and Therapy

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Excess glucose induces hypoxia ...... metabolism and cell migration

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Feng Wang

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Huijie Xiao

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Johan Permert

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Karl-Gösta Sundqvist

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Xiaohui Jia

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Yijie Duan

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Zhiwen Liu

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P2860

A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation

On the Origin of Cancer Cells

Overexpression of hypoxia-inducible factor 1alpha in common human cancers and their metastases

HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption

Hypoxia-inducible factor 1alpha (HIF-1alpha) protein is rapidly degraded by the ubiquitin-proteasome system under normoxic conditions. Its stabilization by hypoxia depends on redox-induced changes

Akt and c-Myc differentially activate cellular metabolic programs and prime cells to bioenergetic inhibition.

Inhibition of hypoxia-inducible factor (HIF) hydroxylases by citric acid cycle intermediates: possible links between cell metabolism and stabilization of HIF.

Resveratrol inhibits cancer cell metabolism by down regulating pyruvate kinase M2 via inhibition of mammalian target of rapamycin.

Reactive oxygen species produced by NAD(P)H oxidase inhibit apoptosis in pancreatic cancer cells.

Pancreatic cancer is associated with impaired glucose metabolism.

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10.4161/CBT.23786

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