High glucose levels promote the proliferation of breast cancer cells through GTPases
Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high gl...
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Published in | Breast cancer targets and therapy Vol. 9; pp. 429 - 436 |
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Abstract | Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia. |
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AbstractList | Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia. Keyword: hyperglycemia, breast cancer, GTPases, Rac1, Cdc42, EGFR Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia.Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia. Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia. Yilin Hou,1 Man Zhou,1 Jing Xie,1 Ping Chao,1 Qiyu Feng,2 Jun Wu1 1Department of Endocrinology, The Third Hospital of Wuhan (Tongren Hospital of Wuhan University), Wuhan, People's Republic of China; 2Eastern Hepatobiliary Surgery Institute, National Center for Liver Cancer, Shanghai, People's Republic of China Abstract: Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years. However, the underlying molecular mechanisms of the pathophysiological link are not yet fully understood. In this study, we demonstrate that high glucose levels promote the proliferation of breast cancer cells by stimulating epidermal growth factor receptor (EGFR) activation and the Rho family GTPase Rac1 and Cdc42 mediate the corresponding signaling induced by high glucose levels. We further show that Cdc42 promotes EGFR phosphorylation by blocking EGFR degradation, which may be mediated by the Cbl proteins, whereas the Rac1-mediated EGFR phosphorylation is independent of EGFR degradation. Our findings elucidate a part of the underlying molecular mechanism of the link between high glucose levels and tumorigenesis in breast cancer and may provide new insights on the therapeutic strategy for cancer patients with diabetes or hyperglycemia. Keyword: hyperglycemia, breast cancer, GTPases, Rac1, Cdc42, EGFR |
Audience | Academic |
Author | Chao, Ping Wu, Jun Xie, Jing Hou, Yilin Zhou, Man Feng, Qiyu |
AuthorAffiliation | 2 Eastern Hepatobiliary Surgery Institute, National Center for Liver Cancer, Shanghai, People’s Republic of China 1 Department of Endocrinology, The Third Hospital of Wuhan (Tongren Hospital of Wuhan University), Wuhan, People’s Republic of China |
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Keywords | hyperglycemia breast cancer Rac1 GTPases EGFR Cdc42 |
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References | 2981413 - Nature. 1985 Jan 10-18;313(5998):144-7 19620249 - Endocr Relat Cancer. 2009 Dec;16(4):1103-23 19307509 - J Clin Oncol. 2009 May 1;27(13):2170-6 22087246 - PLoS One. 2011;6(11):e27074 23606532 - EMBO Mol Med. 2013 May;5(5):723-36 16105029 - Kidney Int. 2005 Sep;68(3):985-97 7536630 - Cell. 1995 Apr 7;81(1):53-62 16377102 - Gene. 2006 Jan 17;366(1):2-16 16061648 - Cancer Res. 2005 Aug 1;65(15):6676-84 8394672 - Anticancer Res. 1993 Jul-Aug;13(4):1133-7 12379472 - Biochim Biophys Acta. 2002 Oct 21;1592(2):107-16 21665891 - Carcinogenesis. 2011 Sep;32(9):1381-7 15644546 - JAMA. 2005 Jan 12;293(2):194-202 24587242 - PLoS One. 2014 Feb 28;9(2):e90136 16407834 - Oncogene. 2006 May 18;25(21):3071-8 24613967 - Small GTPases. 2014;5:e28102 23153508 - Int J Biochem Cell Biol. 2013 Feb;45(2):255-64 21516129 - Oncogene. 2011 Jul 28;30(30):3305-16 20804725 - Biochim Biophys Acta. 2011 Jun;1807(6):577-94 10635327 - Mol Cell. 1999 Dec;4(6):1029-40 11357143 - Nature. 2001 May 17;411(6835):355-65 20960036 - Mol Cell Biochem. 2011 Jan;347(1-2):95-101 7891688 - Mol Cell Biol. 1995 Apr;15(4):1942-52 25254953 - PLoS One. 2014 Sep 25;9(9):e108444 16892055 - Nat Cell Biol. 2006 Sep;8(9):945-56 7892601 - Science. 1995 Mar 24;267(5205):1782-8 21115865 - J Clin Oncol. 2011 Jan 1;29(1):40-6 10514377 - Science. 1999 Oct 8;286(5438):309-12 22019750 - Minerva Endocrinol. 2011 Sep;36(3):187-209 14505571 - Cell. 2003 Sep 19;114(6):715-25 10449615 - Int J Cancer. 1999 Sep 24;83(1):98-106 23942551 - Diabetes. 2013 Nov;62(11):3874-86 24458840 - Stem Cells. 2014 May;32(5):1124-35 |
References_xml | – reference: 24458840 - Stem Cells. 2014 May;32(5):1124-35 – reference: 16061648 - Cancer Res. 2005 Aug 1;65(15):6676-84 – reference: 21516129 - Oncogene. 2011 Jul 28;30(30):3305-16 – reference: 20960036 - Mol Cell Biochem. 2011 Jan;347(1-2):95-101 – reference: 2981413 - Nature. 1985 Jan 10-18;313(5998):144-7 – reference: 10514377 - Science. 1999 Oct 8;286(5438):309-12 – reference: 22087246 - PLoS One. 2011;6(11):e27074 – reference: 24613967 - Small GTPases. 2014;5:e28102 – reference: 25254953 - PLoS One. 2014 Sep 25;9(9):e108444 – reference: 24587242 - PLoS One. 2014 Feb 28;9(2):e90136 – reference: 16407834 - Oncogene. 2006 May 18;25(21):3071-8 – reference: 7891688 - Mol Cell Biol. 1995 Apr;15(4):1942-52 – reference: 22019750 - Minerva Endocrinol. 2011 Sep;36(3):187-209 – reference: 10635327 - Mol Cell. 1999 Dec;4(6):1029-40 – reference: 11357143 - Nature. 2001 May 17;411(6835):355-65 – reference: 19307509 - J Clin Oncol. 2009 May 1;27(13):2170-6 – reference: 23606532 - EMBO Mol Med. 2013 May;5(5):723-36 – reference: 14505571 - Cell. 2003 Sep 19;114(6):715-25 – reference: 10449615 - Int J Cancer. 1999 Sep 24;83(1):98-106 – reference: 23942551 - Diabetes. 2013 Nov;62(11):3874-86 – reference: 16892055 - Nat Cell Biol. 2006 Sep;8(9):945-56 – reference: 7892601 - Science. 1995 Mar 24;267(5205):1782-8 – reference: 16377102 - Gene. 2006 Jan 17;366(1):2-16 – reference: 20804725 - Biochim Biophys Acta. 2011 Jun;1807(6):577-94 – reference: 21115865 - J Clin Oncol. 2011 Jan 1;29(1):40-6 – reference: 23153508 - Int J Biochem Cell Biol. 2013 Feb;45(2):255-64 – reference: 21665891 - Carcinogenesis. 2011 Sep;32(9):1381-7 – reference: 7536630 - Cell. 1995 Apr 7;81(1):53-62 – reference: 12379472 - Biochim Biophys Acta. 2002 Oct 21;1592(2):107-16 – reference: 15644546 - JAMA. 2005 Jan 12;293(2):194-202 – reference: 19620249 - Endocr Relat Cancer. 2009 Dec;16(4):1103-23 – reference: 16105029 - Kidney Int. 2005 Sep;68(3):985-97 – reference: 8394672 - Anticancer Res. 1993 Jul-Aug;13(4):1133-7 |
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Snippet | Hyperglycemia or diabetes mellitus (DM), which is characterized by high blood glucose levels, has been linked to an increased risk of cancer for years.... Yilin Hou,1 Man Zhou,1 Jing Xie,1 Ping Chao,1 Qiyu Feng,2 Jun Wu1 1Department of Endocrinology, The Third Hospital of Wuhan (Tongren Hospital of Wuhan... |
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SubjectTerms | Brain cancer Breast cancer Care and treatment Cdc42 Cell culture Cell cycle Cell growth Development and progression Diabetes EGFR Epidermal growth factor Genetic aspects Glucose Glucose metabolism GTPases Guanosine triphosphatase Health aspects Hyperglycemia Kinases Original Research Phosphorylation Proteins Rac1 Statistical analysis |
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Title | High glucose levels promote the proliferation of breast cancer cells through GTPases |
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