Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer

Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is as...
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Gespeichert in:

Autor*in:	Steven G. Gray [verfasserIn] Calen Sacevich [verfasserIn] Lisa Kilmartin [verfasserIn] Jennifer Leonard [verfasserIn] Anne-Marie Baird [verfasserIn] Kenneth J. O'Byrne [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	NSCLC Glucose transporter epigenetics

Übergeordnetes Werk:	In: Cancers - MDPI AG, 2010, 3(2011), 2, Seite 1550-1565
Übergeordnetes Werk:	volume:3 ; year:2011 ; number:2 ; pages:1550-1565

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cancers3021550

Katalog-ID:	DOAJ063157454

Internformat


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spelling	10.3390/cancers3021550 doi (DE-627)DOAJ063157454 (DE-599)DOAJc2492b9c30344153b2ca34d6c39ae8b9 DE-627 ger DE-627 rakwb eng RC254-282 Steven G. Gray verfasserin aut Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy. NSCLC Glucose transporter epigenetics Neoplasms. Tumors. Oncology. Including cancer and carcinogens Calen Sacevich verfasserin aut Lisa Kilmartin verfasserin aut Jennifer Leonard verfasserin aut Anne-Marie Baird verfasserin aut Kenneth J. O'Byrne verfasserin aut In Cancers MDPI AG, 2010 3(2011), 2, Seite 1550-1565 (DE-627)614095670 (DE-600)2527080-1 20726694 nnns volume:3 year:2011 number:2 pages:1550-1565 https://doi.org/10.3390/cancers3021550 kostenfrei https://doaj.org/article/c2492b9c30344153b2ca34d6c39ae8b9 kostenfrei http://www.mdpi.com/2072-6694/3/2/1550/ kostenfrei https://doaj.org/toc/2072-6694 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2011 2 1550-1565
allfields_unstemmed	10.3390/cancers3021550 doi (DE-627)DOAJ063157454 (DE-599)DOAJc2492b9c30344153b2ca34d6c39ae8b9 DE-627 ger DE-627 rakwb eng RC254-282 Steven G. Gray verfasserin aut Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy. NSCLC Glucose transporter epigenetics Neoplasms. Tumors. Oncology. Including cancer and carcinogens Calen Sacevich verfasserin aut Lisa Kilmartin verfasserin aut Jennifer Leonard verfasserin aut Anne-Marie Baird verfasserin aut Kenneth J. O'Byrne verfasserin aut In Cancers MDPI AG, 2010 3(2011), 2, Seite 1550-1565 (DE-627)614095670 (DE-600)2527080-1 20726694 nnns volume:3 year:2011 number:2 pages:1550-1565 https://doi.org/10.3390/cancers3021550 kostenfrei https://doaj.org/article/c2492b9c30344153b2ca34d6c39ae8b9 kostenfrei http://www.mdpi.com/2072-6694/3/2/1550/ kostenfrei https://doaj.org/toc/2072-6694 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2011 2 1550-1565
allfieldsGer	10.3390/cancers3021550 doi (DE-627)DOAJ063157454 (DE-599)DOAJc2492b9c30344153b2ca34d6c39ae8b9 DE-627 ger DE-627 rakwb eng RC254-282 Steven G. Gray verfasserin aut Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy. NSCLC Glucose transporter epigenetics Neoplasms. Tumors. Oncology. Including cancer and carcinogens Calen Sacevich verfasserin aut Lisa Kilmartin verfasserin aut Jennifer Leonard verfasserin aut Anne-Marie Baird verfasserin aut Kenneth J. O'Byrne verfasserin aut In Cancers MDPI AG, 2010 3(2011), 2, Seite 1550-1565 (DE-627)614095670 (DE-600)2527080-1 20726694 nnns volume:3 year:2011 number:2 pages:1550-1565 https://doi.org/10.3390/cancers3021550 kostenfrei https://doaj.org/article/c2492b9c30344153b2ca34d6c39ae8b9 kostenfrei http://www.mdpi.com/2072-6694/3/2/1550/ kostenfrei https://doaj.org/toc/2072-6694 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2011 2 1550-1565
allfieldsSound	10.3390/cancers3021550 doi (DE-627)DOAJ063157454 (DE-599)DOAJc2492b9c30344153b2ca34d6c39ae8b9 DE-627 ger DE-627 rakwb eng RC254-282 Steven G. Gray verfasserin aut Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy. NSCLC Glucose transporter epigenetics Neoplasms. Tumors. Oncology. Including cancer and carcinogens Calen Sacevich verfasserin aut Lisa Kilmartin verfasserin aut Jennifer Leonard verfasserin aut Anne-Marie Baird verfasserin aut Kenneth J. O'Byrne verfasserin aut In Cancers MDPI AG, 2010 3(2011), 2, Seite 1550-1565 (DE-627)614095670 (DE-600)2527080-1 20726694 nnns volume:3 year:2011 number:2 pages:1550-1565 https://doi.org/10.3390/cancers3021550 kostenfrei https://doaj.org/article/c2492b9c30344153b2ca34d6c39ae8b9 kostenfrei http://www.mdpi.com/2072-6694/3/2/1550/ kostenfrei https://doaj.org/toc/2072-6694 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2011 2 1550-1565
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callnumber-first	R - Medicine
author	Steven G. Gray
spellingShingle	Steven G. Gray misc RC254-282 misc NSCLC misc Glucose transporter misc epigenetics misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer
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topic_title	RC254-282 Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer NSCLC Glucose transporter epigenetics
topic	misc RC254-282 misc NSCLC misc Glucose transporter misc epigenetics misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc NSCLC misc Glucose transporter misc epigenetics misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc NSCLC misc Glucose transporter misc epigenetics misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer
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title_full	Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer
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title_sort	epigenetic regulation of glucose transporters in non-small cell lung cancer
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title_auth	Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer
abstract	Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy.
abstractGer	Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy.
abstract_unstemmed	Due to their inherently hypoxic environment, cancer cells often resort to glycolysis, or the anaerobic breakdown of glucose to form ATP to provide for their energy needs, known as the Warburg effect. At the same time, overexpression of the insulin receptor in non-small cell lung cancer (NSCLC) is associated with an increased risk of metastasis and decreased survival. The uptake of glucose into cells is carried out via glucose transporters or GLUTs. Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Following treatment with the epigenetic targeting agents histone deacetylase inhibitors (HDACi), GLUT-3 and GLUT-4 expression were found to be induced in NSCLC cell lines, with minimal responses in transformed normal human bronchial epithelial cells (HBECs). Similar results for GLUT-4 were observed in cells derived from liver, muscle, kidney and pre-adipocytes. Bioinformatic analysis of the promoter for GLUT-4 indicates that it may also be regulated by several chromatin binding factors or complexes including CTCF, SP1 and SMYD3. Chromatin immunoprecipitation studies demonstrate that the promoter for GLUT-4 is dynamically remodeled in response to HDACi. Overall, these results may have value within the clinical setting as (a) it may be possible to use this to enhance fluorodeoxyglucose (18F) positron emission tomography (FDG-PET) imaging sensitivity; (b) it may be possible to target NSCLC through the use of HDACi and insulin mediated uptake of the metabolic targeting drugs such as 2-deoxyglucose (2-DG); or (c) enhance or sensitize NSCLC to chemotherapy.
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title_short	Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer
url	https://doi.org/10.3390/cancers3021550 https://doaj.org/article/c2492b9c30344153b2ca34d6c39ae8b9 http://www.mdpi.com/2072-6694/3/2/1550/ https://doaj.org/toc/2072-6694
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up_date	2024-07-03T16:09:38.782Z
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Epigenetic Regulation of Glucose Transporters in Non-Small Cell Lung Cancer

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