AMP-Activated Protein Kinase Upregulates Glucose Uptake in Thyroid PCCL3 Cells Independent of Thyrotropin

Andrade, Bruno Geike de; Cazarin, Juliana; Zancan, Patrícia; Carvalho, Denise P.

doi:10.1089/thy.2012.0041

Cited by 24 publications

(31 citation statements)

References 17 publications

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“…Thyroid cancer cells also show a high rate of glycolysis (Andrade et al 2012). Immunohistochemical studies have shown that enhanced glucose uptake in cancer cells correlates with over-expression of GLUTs, in most cases GLUT1 (Haber et al 1997, Ciampi et al 2008.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the absence of glucose is 'dominant' in driving GLUT1 membrane translocation, regardless of the presence of PTEN as in fact occurs in WRO cells as well (Figs 2C,4 and 6B). Glucose depletion is known to activate the AMPK pathway, which is also involved in the membrane expression of GLUT1 (Andrade et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…There are indications that the surface expression of GLUT proteins is under the control of the phosphoinositide 3-kinase (PI3K)/AKT pathway (Samih et al 2000). Recently, AMPK has been shown to play a pivotal role in the membrane expression of GLUT1 and glucose uptake in rat follicular thyroid cells (Andrade et al 2012). In a small cohort of patients, we found that loss of expression of the oncosuppressor PTEN, a protein-lipid phosphatase that switches off the AKT pathway, was associated with an increased probability of detecting thyroid incidentalomas by FDG-PET (Morani et al 2012).…”

Section: Introductionmentioning

confidence: 99%

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PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

Morani

Phadngam

Follo

et al. 2014

Journal of Molecular Endocrinology

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Glucose represents an important source of energy for the cells. Proliferating cancer cells consume elevated quantity of glucose, which is converted into lactate regardless of the presence of oxygen. This phenomenon, known as the Warburg effect, has been proven to be useful for imaging metabolically active tumours in cancer patients by 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET). Glucose is internalised in the cells by glucose transporters (GLUTs) belonging to the GLUT family. GLUT1 (SLC2A1) is the most prevalent isoform in more aggressive and less differentiated thyroid cancer histotypes. In a previous work, we found that loss of expression of PTEN was associated with increased expression of GLUT1 on the plasma membrane (PM) and probability of detecting thyroid incidentalomas by FDG-PET. Herein, we investigated the molecular pathways that govern the expression of GLUT1 on the PM and the glucose uptake in WRO (expressing WT PTEN) and FTC133 (PTEN null) follicular thyroid cancer cells cultured under glucose-depleted conditions. The membrane expression of GLUT1 was enhanced in glucose-deprived cells. Through genetic manipulations of PTEN expression, we could demonstrate that the lack of this oncosuppressor has a dominant effect on the membrane expression of GLUT1 and glucose uptake. We conclude that loss of function of PTEN increases the probability of cancer detection by FDG-PET or other glucose-based imaging diagnosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

Morani

Phadngam

Follo

et al. 2014

Journal of Molecular Endocrinology

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“…Recently, we described that the AMPK plays an important physiological role in the thyroid gland by regulating uptake of both iodide and glucose (Andrade et al 2011(Andrade et al , 2012. In fact, AMPK activation in the normal thyrocyte induces a dramatic reduction of iodide uptake that is accompanied by a higher glucose uptake and glycolytic pathway utilization.…”

Section: The Role Of 18 F-fdg-pet/ctmentioning

confidence: 99%

A new appraisal of iodine refractory thyroid cancer

Vaisman¹,

Carvalho²,

Vaisman³

2015

Endocrine-Related Cancer

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Thyroid cancer incidence is increasing all over the world -mostly due to an increase in the detection of small tumors that were previously undetected. A small percentage of these tumors lose the ability to uptake and/or to respond to radioiodine (RAI) therapy, especially in metastatic patients. There are several new therapeutic options that have emerged in the last 5 years to treat RAI refractory thyroid cancer patients, however, it is very important to properly identify RAI refractory patients and to clarify those appropriate for these treatments. In this review, we discuss the RAI refractory definitions and the criteria that have been suggested based on RAI uptake in the post therapy scan, as well as the response after RAI therapy and the possible molecular mechanisms involved in this process. We offer a review of the therapeutic options available at the moment and the therapeutic considerations based on a patient's individualized personal characteristics, primary tumor histology, tumor burden and location and velocity of lesion growth.

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“…In its activated state, AMPK allows cellular adaptive changes in order to maintain growth, differentiation, and metabolism under conditions of low intracellular energy availability (1,2,3,4,5). Recently, we described the involvement of AMPK signaling in the regulation of iodide and glucose uptake in rat thyrocytes, both in vitro and in vivo (3,6). We showed that the AMPK activator, 5-aminoimidazole-4-carboxamideribonucleoside (AICAR), decreases iodide uptake (in vitro and in vivo) and NIS protein and mRNA content in thyroid cells (4).…”

Section: Introductionmentioning

confidence: 99%

AMP-activated protein kinase signaling is upregulated in papillary thyroid cancer

Vidal

Andrade

Vaisman

et al. 2013

European Journal of Endocrinology

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AMP-activated protein kinase (AMPK) is activated by the depletion in cellular energy levels and allows adaptive changes in cell metabolism and cell survival. Recently, our group described that AMPK plays an important role in the regulation of iodide and glucose uptake in thyroid cells. However, AMPK signaling pathway in human thyroid carcinomas has not been investigated so far. Objective: To evaluate the expression and activity of AMPK in papillary thyroid carcinomas. Methods: We examined total and phosphorylated AMPK (tAMPK and pAMPK) and phosphorylated acetyl-CoA-carboxylase (pACC) expressions through imunohistochemistry, using a tissue microarray block composed of 73 papillary thyroid carcinomas (PAP CA) or microcarcinomas (PAP MCA) and six adenoma (AD) samples from patients followed at the Federal University Hospital. The expression levels were compared with the non-neoplastic tissues from the same patient. Two different pathologists analyzed the samples and attributed scores of staining intensity and the proportion of stained cells. A total index was obtained by multiplying the values of intensity and the proportion of stained cells (INTxPROP). Results: tAMPK, pAMPK, and pACC showed a predominant cytoplasmic staining in papillary carcinomas, adenomas, and non-neoplastic thyroid tissues. However, the intensity and the proportion of stained cells were higher in carcinomas, so that a significant increase was found in the INTxPROP score both in PAP CA and PAP MCA, when compared with their respective controls. Conclusion: Our results show unequivocally that AMPK pathway is highly activated in papillary thyroid carcinomas; however, more studies are necessary to understand the pathophysiological significance of AMPK activation in thyroid carcinogenesis.

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AMP-Activated Protein Kinase Upregulates Glucose Uptake in Thyroid PCCL3 Cells Independent of Thyrotropin

Abstract: Our results show that AMPK activation significantly upregulates GLUT 1 content and glucose uptake, and it also stimulates hexokinase activity, the first step of glycolysis.

Cited by 24 publications

References 17 publications

PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

A new appraisal of iodine refractory thyroid cancer

AMP-activated protein kinase signaling is upregulated in papillary thyroid cancer

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