IGF-1 controls GLUT3 expression in muscle via the transcriptional factor Sp1

Copland, John A.; Pardini, Aaron W.; Wood, Thomas G.; Yin, Deling; Green, Allan; Bodenburg, Yvonne H.; Urban, Randall J.; Stuart, Charles Alexander

doi:10.1016/j.bbaexp.2007.08.002

Cited by 20 publications

(15 citation statements)

References 27 publications

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“…In rat neurons, Sp1 and Sp3 regulated GLUT3 expression and bound to cis elements in the promoter (22,23). In mouse muscle cells, insulin-like growth factor-I played a role in maintaining GLUT3 expression via Sp1 (24). The mouse GLUT3 promoter also responded to cyclic AMP in a breast cancer cell line (25).…”

Section: Introductionmentioning

confidence: 84%

DNA Damage–Induced Modulation of GLUT3 Expression Is Mediated through p53-Independent Extracellular Signal-Regulated Kinase Signaling in HeLa Cells

Watanabe

Naraba

Sakyo

et al. 2010

Molecular Cancer Research

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Many cancer cells exhibit increased rates of uptake and metabolism of glucose compared with normal cells. Glucose uptake in mammalian cells is mediated by the glucose transporter (GLUT) family. Here, we report that DNA-damaging anticancer agents such as Adriamycin and etoposide suppressed the expression of GLUT3, but not GLUT1, in HeLa cells and a tumorigenic HeLa cell hybrid. Suppression of GLUT3 expression determined by the real-time PCR was also evident with another DNA-damaging agent, camptothecin, which reduced the promoter's activity as determined with a luciferase-linked assay. The suppression by these agents seemed to be induced independently of p53, and it was evident when wild-type p53 was overproduced in these cells. In contrast, the mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) kinase (MEK) inhibitor U0126 (but not the phosphoinositide 3-kinase inhibitor LY294002) prevented the drug-induced suppression as determined by reverse transcription-PCR and promoter assays. Furthermore, overexpression of GLUT3 in HeLa cell hybrids increased resistance to these drugs, whereas depletion of the gene by small interfering RNA rendered the cells more sensitive to the drugs, decreasing glucose consumption. The results suggest that DNA-damaging agents reduce GLUT3 expression in cancer cells through activation of the MEK-ERK pathway independently of p53, leading to cell death or apoptosis. The findings may contribute to the development of new chemotherapeutic drugs based on the GLUT3-dependent metabolism of glucose.

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Section: Introductionmentioning

confidence: 84%

DNA Damage–Induced Modulation of GLUT3 Expression Is Mediated through p53-Independent Extracellular Signal-Regulated Kinase Signaling in HeLa Cells

Watanabe

Naraba

Sakyo

et al. 2010

Molecular Cancer Research

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“…Extensive sitespecific mutagenesis experiments revealed that functional interactions among all four Sp1 sites were obligatory for optimal transcription of IR in response to glucose and insulin (Fukuda et al, 2001). In a related study, Copland et al (2007) showed that insulin like growth factor-1-mediated regulation of glucose transport (GLUT3) gene expression in the skeletal muscle was mediated by transcription factor Sp1; co-transfection of L6 muscle cells by GLUT3 promoter- luciferease and Sp1 expression plasmid greatly enhanced the expression of the reporter luciferase (Samson and Wong, 2002).…”

Section: Role Of Sp1 As a Putative Transducer Of Insulin Signaling Inmentioning

confidence: 98%

A critical role of Sp1 transcription factor in regulating gene expression in response to insulin and other hormones

et al. 2008

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“…In addition to decreasing inflammation and stimulating regeneration of new WAT, IGF-I may also contribute to glucose homeostasis through insulin-independent glucose uptake into peripheral tissues via GLUT1 and GLUT3 glucose transporters (9,15,82) as well as direct activation of the insulin receptor. There is considerable structural similarity between the receptors for insulin and IGF-I (29,38).…”

Section: Discussionmentioning

confidence: 99%

Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

Gunawardana

Piston

2015

American Journal of Physiology-Endocrinology and Metabolism

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Gunawardana SC, Piston DW. Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant. Am J Physiol Endocrinol Metab 308: E1043-E1055, 2015. First published April 21, 2015; doi:10.1152/ajpendo.00570.2014.-Traditional therapies for type 1 diabetes (T1D) involve insulin replacement or islet/pancreas transplantation and have numerous limitations. Our previous work demonstrated the ability of embryonic brown adipose tissue (BAT) transplants to establish normoglycemia without insulin in chemically induced models of insulin-deficient diabetes. The current study sought to extend the technique to an autoimmune-mediated T1D model and document the underlying mechanisms. In nonobese diabetic (NOD) mice, BAT transplants result in complete reversal of T1D associated with rapid and longlasting euglycemia. In addition, BAT transplants placed prior to the onset of diabetes on NOD mice can prevent or significantly delay the onset of diabetes. As with streptozotocin (STZ)-diabetic models, euglycemia is independent of insulin and strongly correlates with decrease of inflammation and increase of adipokines. Plasma insulinlike growth factor-I (IGF-I) is the first hormone to increase following BAT transplants. Adipose tissue of transplant recipients consistently express IGF-I compared with little or no expression in controls, and plasma IGF-I levels show a direct negative correlation with glucose, glucagon, and inflammatory cytokines. Adipogenic and anti-inflammatory properties of IGF-I may stimulate regeneration of new healthy white adipose tissue, which in turn secretes hypoglycemic adipokines that substitute for insulin. IGF-I can also directly decrease blood glucose through activating insulin receptor. These data demonstrate the potential for insulin-independent reversal of autoimmune-induced T1D with BAT transplants and implicate IGF-I as a likely mediator in the resulting equilibrium. type 1 diabetes; brown adipose tissue; insulin independent; transplantation; insulin-like growth factor I TYPE 1 DIABETES (T1D) is characterized by autoimmune-mediated destruction of pancreatic ␤-cells, resulting in absolute deficiency of insulin and loss of glycemic control. Treatments for T1D, despite having been refined over many years, are geared mainly toward replacing insulin, which involves numerous risks and limitations. Direct insulin replacement via daily injections or insulin pump does not cure the disease and requires life-long repeated administration. In addition to the inconvenience, direct insulin therapy requires careful monitoring of dosage and blood glucose levels and can lead to potentially fatal hypoglycemic episodes. Pancreas transplantation, the only available treatment with a good chance of long-term insulin independence, requires invasive surgery and life-long immunosuppressive therapy. Islet transplantation, although less invasive, is limited by the availability of donor tissue and the need for immunosuppression, and patients often return to insulin dependence in the long...

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IGF-1 controls GLUT3 expression in muscle via the transcriptional factor Sp1

Cited by 20 publications

References 27 publications

DNA Damage–Induced Modulation of GLUT3 Expression Is Mediated through p53-Independent Extracellular Signal-Regulated Kinase Signaling in HeLa Cells

DNA Damage–Induced Modulation of GLUT3 Expression Is Mediated through p53-Independent Extracellular Signal-Regulated Kinase Signaling in HeLa Cells

A critical role of Sp1 transcription factor in regulating gene expression in response to insulin and other hormones

Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

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