High glucose levels promote the proliferation of breast cancer cells through GTPases

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, Peopl...

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Autores principales:	Hou Y, Zhou M, Xie J, Chao P, Feng Q, Wu J
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2017
Materias:	Hyperglycemia Breast cancer GTPases Rac1 Cdc42 EGFR Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/bc369f12f9214f6fbbf7e78b375cb31a
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spelling	oai:doaj.org-article:bc369f12f9214f6fbbf7e78b375cb31a2021-12-02T03:03:27ZHigh glucose levels promote the proliferation of breast cancer cells through GTPases1179-1314https://doaj.org/article/bc369f12f9214f6fbbf7e78b375cb31a2017-06-01T00:00:00Zhttps://www.dovepress.com/high-glucose-levels-promote-the-proliferation-of-breast-cancer-cells-t-peer-reviewed-article-BCTThttps://doaj.org/toc/1179-1314Yilin 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, EGFRHou YZhou MXie JChao PFeng QWu JDove Medical PressarticleHyperglycemiaBreast cancerGTPasesRac1Cdc42EGFRNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENBreast Cancer: Targets and Therapy, Vol Volume 9, Pp 429-436 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Hyperglycemia Breast cancer GTPases Rac1 Cdc42 EGFR Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Hyperglycemia Breast cancer GTPases Rac1 Cdc42 EGFR Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Hou Y Zhou M Xie J Chao P Feng Q Wu J High glucose levels promote the proliferation of breast cancer cells through GTPases
description	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
format	article
author	Hou Y Zhou M Xie J Chao P Feng Q Wu J
author_facet	Hou Y Zhou M Xie J Chao P Feng Q Wu J
author_sort	Hou Y
title	High glucose levels promote the proliferation of breast cancer cells through GTPases
title_short	High glucose levels promote the proliferation of breast cancer cells through GTPases
title_full	High glucose levels promote the proliferation of breast cancer cells through GTPases
title_fullStr	High glucose levels promote the proliferation of breast cancer cells through GTPases
title_full_unstemmed	High glucose levels promote the proliferation of breast cancer cells through GTPases
title_sort	high glucose levels promote the proliferation of breast cancer cells through gtpases
publisher	Dove Medical Press
publishDate	2017
url	https://doaj.org/article/bc369f12f9214f6fbbf7e78b375cb31a
work_keys_str_mv	AT houy highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases AT zhoum highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases AT xiej highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases AT chaop highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases AT fengq highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases AT wuj highglucoselevelspromotetheproliferationofbreastcancercellsthroughgtpases
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High glucose levels promote the proliferation of breast cancer cells through GTPases

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