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Diacylglycerol kinase I* modulates oncogenic properties of lung cancer cells.(Report)

Byline: T. Nakano (1), A. Iravani (1,3), M. Kim (1,2), Y. Hozumi (1), M. Lohse (1), E. Reichert (1), T. M. Crotty (1), D. M. Stafforini (1,3), M. K. Topham (1,2,3) Keywords: Diacylglycerol kinase; Epidermal growth factor receptor; Lipid signaling; Diacylglycerol; Lung cancer Abstract: Purpose Lung c... Full description

Journal Title: Clinical and Translational Oncology Jan, 2014, Vol.16(1), p.29(7)
Main Author: Nakano, T.
Other Authors: Iravani, A. , Kim, M. , Hozumi, Y. , Lohse, M. , Reichert, E. , Crotty, T. M. , Stafforini, D. M. , Topham, M. K.
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 1699-048X
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recordid: gale_ofa355013656
title: Diacylglycerol kinase I* modulates oncogenic properties of lung cancer cells.(Report)
format: Article
creator:
  • Nakano, T.
  • Iravani, A.
  • Kim, M.
  • Hozumi, Y.
  • Lohse, M.
  • Reichert, E.
  • Crotty, T. M.
  • Stafforini, D. M.
  • Topham, M. K.
subjects:
  • Lung Cancer -- Analysis
  • Epidermal Growth Factors -- Analysis
  • Cancer Cells -- Analysis
  • Enzymes -- Analysis
ispartof: Clinical and Translational Oncology, Jan, 2014, Vol.16(1), p.29(7)
description: Byline: T. Nakano (1), A. Iravani (1,3), M. Kim (1,2), Y. Hozumi (1), M. Lohse (1), E. Reichert (1), T. M. Crotty (1), D. M. Stafforini (1,3), M. K. Topham (1,2,3) Keywords: Diacylglycerol kinase; Epidermal growth factor receptor; Lipid signaling; Diacylglycerol; Lung cancer Abstract: Purpose Lung cancer is a leading cause of cancer deaths and efforts are underway to identify novel therapies to treat these tumors. Diacylglycerol kinase I* (DGKI*), an enzyme that phosphorylates diacylglycerol to form phosphatidic acid, has been shown to modulate MAPK signaling downstream of EGFR, which is an oncogenic driver in some lung cancers. Since mutations in EGFR and K-Ras are common in lung cancer, we hypothesized that limiting the function of DGKI* would attenuate oncogenic properties of lung cancer cells. Methods We determined the expression levels of DGKI* in a mouse models of mutant EGFR and K-Ras lung cancer and in human lung cancer cell lines with activating mutations in either EGFR or K-Ras. We also tested the effects of shRNA-mediated depletion of DGKI* in lung cancer cells and tested if DGKI* depletion augmented the effects of afatinib, a new generation EGFR inhibitor. Results DGKI* was expressed in malignant epithelium from mice with mutant EGFR or K-Ras lung cancer. It was also expressed in human lung cancer cell lines with EGFR or K-Ras mutations. Depleting DGKI* in lung cancer cell lines, harboring mutant EGFR, reduced their growth on plastic and in soft agar and also augmented the effects of afatinib, an EGFR inhibitor. DGKI* depletion also reduced growth of one of two lung cancer cell lines that harbored mutant K-Ras. Conclusions Our data indicate that DGKI* is a potential therapeutic target in lung cancers, especially those harboring EGFR mutations. Our findings warrant further studies to examine the effects of limiting its function in vivo. Author Affiliation: (1) Huntsman Cancer Institute, University of Utah, 2000 East Circle of Hope, Salt Lake City, UT, 84112-5550, USA (2) Department of Oncological Sciences, University of Utah, Salt Lake City, UT, 84112, USA (3) Department of Internal Medicine, University of Utah, Salt Lake City, UT, 84112, USA Article History: Registration Date: 26/03/2013 Received Date: 10/10/2012 Accepted Date: 26/03/2013 Online Date: 10/04/2013 Article note: T. Nakano and A. Iravani contributed equally to this manuscript.
language: English
source: Cengage Learning, Inc.
identifier: ISSN: 1699-048X
fulltext: fulltext
issn:
  • 1699-048X
  • 1699048X
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titleDiacylglycerol kinase I* modulates oncogenic properties of lung cancer cells.(Report)
creatorNakano, T. ; Iravani, A. ; Kim, M. ; Hozumi, Y. ; Lohse, M. ; Reichert, E. ; Crotty, T. M. ; Stafforini, D. M. ; Topham, M. K.
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subjectLung Cancer -- Analysis ; Epidermal Growth Factors -- Analysis ; Cancer Cells -- Analysis ; Enzymes -- Analysis
descriptionByline: T. Nakano (1), A. Iravani (1,3), M. Kim (1,2), Y. Hozumi (1), M. Lohse (1), E. Reichert (1), T. M. Crotty (1), D. M. Stafforini (1,3), M. K. Topham (1,2,3) Keywords: Diacylglycerol kinase; Epidermal growth factor receptor; Lipid signaling; Diacylglycerol; Lung cancer Abstract: Purpose Lung cancer is a leading cause of cancer deaths and efforts are underway to identify novel therapies to treat these tumors. Diacylglycerol kinase I* (DGKI*), an enzyme that phosphorylates diacylglycerol to form phosphatidic acid, has been shown to modulate MAPK signaling downstream of EGFR, which is an oncogenic driver in some lung cancers. Since mutations in EGFR and K-Ras are common in lung cancer, we hypothesized that limiting the function of DGKI* would attenuate oncogenic properties of lung cancer cells. Methods We determined the expression levels of DGKI* in a mouse models of mutant EGFR and K-Ras lung cancer and in human lung cancer cell lines with activating mutations in either EGFR or K-Ras. We also tested the effects of shRNA-mediated depletion of DGKI* in lung cancer cells and tested if DGKI* depletion augmented the effects of afatinib, a new generation EGFR inhibitor. Results DGKI* was expressed in malignant epithelium from mice with mutant EGFR or K-Ras lung cancer. It was also expressed in human lung cancer cell lines with EGFR or K-Ras mutations. Depleting DGKI* in lung cancer cell lines, harboring mutant EGFR, reduced their growth on plastic and in soft agar and also augmented the effects of afatinib, an EGFR inhibitor. DGKI* depletion also reduced growth of one of two lung cancer cell lines that harbored mutant K-Ras. Conclusions Our data indicate that DGKI* is a potential therapeutic target in lung cancers, especially those harboring EGFR mutations. Our findings warrant further studies to examine the effects of limiting its function in vivo. Author Affiliation: (1) Huntsman Cancer Institute, University of Utah, 2000 East Circle of Hope, Salt Lake City, UT, 84112-5550, USA (2) Department of Oncological Sciences, University of Utah, Salt Lake City, UT, 84112, USA (3) Department of Internal Medicine, University of Utah, Salt Lake City, UT, 84112, USA Article History: Registration Date: 26/03/2013 Received Date: 10/10/2012 Accepted Date: 26/03/2013 Online Date: 10/04/2013 Article note: T. Nakano and A. Iravani contributed equally to this manuscript.
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titleDiacylglycerol kinase I* modulates oncogenic properties of lung cancer cells.(Report)
descriptionByline: T. Nakano (1), A. Iravani (1,3), M. Kim (1,2), Y. Hozumi (1), M. Lohse (1), E. Reichert (1), T. M. Crotty (1), D. M. Stafforini (1,3), M. K. Topham (1,2,3) Keywords: Diacylglycerol kinase; Epidermal growth factor receptor; Lipid signaling; Diacylglycerol; Lung cancer Abstract: Purpose Lung cancer is a leading cause of cancer deaths and efforts are underway to identify novel therapies to treat these tumors. Diacylglycerol kinase I* (DGKI*), an enzyme that phosphorylates diacylglycerol to form phosphatidic acid, has been shown to modulate MAPK signaling downstream of EGFR, which is an oncogenic driver in some lung cancers. Since mutations in EGFR and K-Ras are common in lung cancer, we hypothesized that limiting the function of DGKI* would attenuate oncogenic properties of lung cancer cells. Methods We determined the expression levels of DGKI* in a mouse models of mutant EGFR and K-Ras lung cancer and in human lung cancer cell lines with activating mutations in either EGFR or K-Ras. We also tested the effects of shRNA-mediated depletion of DGKI* in lung cancer cells and tested if DGKI* depletion augmented the effects of afatinib, a new generation EGFR inhibitor. Results DGKI* was expressed in malignant epithelium from mice with mutant EGFR or K-Ras lung cancer. It was also expressed in human lung cancer cell lines with EGFR or K-Ras mutations. Depleting DGKI* in lung cancer cell lines, harboring mutant EGFR, reduced their growth on plastic and in soft agar and also augmented the effects of afatinib, an EGFR inhibitor. DGKI* depletion also reduced growth of one of two lung cancer cell lines that harbored mutant K-Ras. Conclusions Our data indicate that DGKI* is a potential therapeutic target in lung cancers, especially those harboring EGFR mutations. Our findings warrant further studies to examine the effects of limiting its function in vivo. Author Affiliation: (1) Huntsman Cancer Institute, University of Utah, 2000 East Circle of Hope, Salt Lake City, UT, 84112-5550, USA (2) Department of Oncological Sciences, University of Utah, Salt Lake City, UT, 84112, USA (3) Department of Internal Medicine, University of Utah, Salt Lake City, UT, 84112, USA Article History: Registration Date: 26/03/2013 Received Date: 10/10/2012 Accepted Date: 26/03/2013 Online Date: 10/04/2013 Article note: T. Nakano and A. Iravani contributed equally to this manuscript.
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abstractByline: T. Nakano (1), A. Iravani (1,3), M. Kim (1,2), Y. Hozumi (1), M. Lohse (1), E. Reichert (1), T. M. Crotty (1), D. M. Stafforini (1,3), M. K. Topham (1,2,3) Keywords: Diacylglycerol kinase; Epidermal growth factor receptor; Lipid signaling; Diacylglycerol; Lung cancer Abstract: Purpose Lung cancer is a leading cause of cancer deaths and efforts are underway to identify novel therapies to treat these tumors. Diacylglycerol kinase I* (DGKI*), an enzyme that phosphorylates diacylglycerol to form phosphatidic acid, has been shown to modulate MAPK signaling downstream of EGFR, which is an oncogenic driver in some lung cancers. Since mutations in EGFR and K-Ras are common in lung cancer, we hypothesized that limiting the function of DGKI* would attenuate oncogenic properties of lung cancer cells. Methods We determined the expression levels of DGKI* in a mouse models of mutant EGFR and K-Ras lung cancer and in human lung cancer cell lines with activating mutations in either EGFR or K-Ras. We also tested the effects of shRNA-mediated depletion of DGKI* in lung cancer cells and tested if DGKI* depletion augmented the effects of afatinib, a new generation EGFR inhibitor. Results DGKI* was expressed in malignant epithelium from mice with mutant EGFR or K-Ras lung cancer. It was also expressed in human lung cancer cell lines with EGFR or K-Ras mutations. Depleting DGKI* in lung cancer cell lines, harboring mutant EGFR, reduced their growth on plastic and in soft agar and also augmented the effects of afatinib, an EGFR inhibitor. DGKI* depletion also reduced growth of one of two lung cancer cell lines that harbored mutant K-Ras. Conclusions Our data indicate that DGKI* is a potential therapeutic target in lung cancers, especially those harboring EGFR mutations. Our findings warrant further studies to examine the effects of limiting its function in vivo. Author Affiliation: (1) Huntsman Cancer Institute, University of Utah, 2000 East Circle of Hope, Salt Lake City, UT, 84112-5550, USA (2) Department of Oncological Sciences, University of Utah, Salt Lake City, UT, 84112, USA (3) Department of Internal Medicine, University of Utah, Salt Lake City, UT, 84112, USA Article History: Registration Date: 26/03/2013 Received Date: 10/10/2012 Accepted Date: 26/03/2013 Online Date: 10/04/2013 Article note: T. Nakano and A. Iravani contributed equally to this manuscript.
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