Hyperglycemia-induced oxidative stress promotes tumor metastasis by upregulating vWF expression in endothelial cells through the transcription factor GATA1
Diabetes mellitus (DM) characterized by hyperglycemia is a chronic metabolic disorder that leads to many symptoms and vascular complications. Despite the close association between DM and cancer progression, the response and role of endothelial cells (ECs) under diabetic conditions in tumor metastasi...
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Published in | Oncogene Vol. 41; no. 11; pp. 1634 - 1646 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group UK
10.03.2022
Nature Publishing Group |
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Abstract | Diabetes mellitus (DM) characterized by hyperglycemia is a chronic metabolic disorder that leads to many symptoms and vascular complications. Despite the close association between DM and cancer progression, the response and role of endothelial cells (ECs) under diabetic conditions in tumor metastasis remain to be elucidated. In this study, we sought to determine whether and how ECs under diabetic conditions contribute to tumor metastasis. We have taken advantage of syngeneic mouse tumor models of Lewis lung carcinoma (LLC) and melanoma (B16F10) cells and a streptozotocin (STZ)-induced hyperglycemia model. We demonstrated that hyperglycemia increased the metastasis of LLC and B16F10 cells in an experimental metastasis model with an intravenous injection of the tumor cells. We also found that hyperglycemia promoted lung metastasis of tumor cells by increasing the adhesiveness of ECs to facilitate the adhesion of tumor cells to ECs rather than affecting the metastatic behavior of tumor cells themselves. From the analysis of gene expression in primary lung ECs from STZ-treated mice, we identified that vWF promoted the adhesion of tumor cells to ECs and the transendothelial migration of tumor cells. Mechanistically, hyperglycemia-induced oxidative stress in ECs, and increased oxidative stress enhanced vWF expression in ECs through an increase in the transcription factor GATA1. These results provide evidence for the role of vWF in ECs in promoting hyperglycemia-induced tumor metastasis and potential therapeutic targets for the regulation of vWF expression in ECs and hyperglycemia-induced tumor metastasis. |
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AbstractList | Diabetes mellitus (DM) characterized by hyperglycemia is a chronic metabolic disorder that leads to many symptoms and vascular complications. Despite the close association between DM and cancer progression, the response and role of endothelial cells (ECs) under diabetic conditions in tumor metastasis remain to be elucidated. In this study, we sought to determine whether and how ECs under diabetic conditions contribute to tumor metastasis. We have taken advantage of syngeneic mouse tumor models of Lewis lung carcinoma (LLC) and melanoma (B16F10) cells and a streptozotocin (STZ)-induced hyperglycemia model. We demonstrated that hyperglycemia increased the metastasis of LLC and B16F10 cells in an experimental metastasis model with an intravenous injection of the tumor cells. We also found that hyperglycemia promoted lung metastasis of tumor cells by increasing the adhesiveness of ECs to facilitate the adhesion of tumor cells to ECs rather than affecting the metastatic behavior of tumor cells themselves. From the analysis of gene expression in primary lung ECs from STZ-treated mice, we identified that vWF promoted the adhesion of tumor cells to ECs and the transendothelial migration of tumor cells. Mechanistically, hyperglycemia-induced oxidative stress in ECs, and increased oxidative stress enhanced vWF expression in ECs through an increase in the transcription factor GATA1. These results provide evidence for the role of vWF in ECs in promoting hyperglycemia-induced tumor metastasis and potential therapeutic targets for the regulation of vWF expression in ECs and hyperglycemia-induced tumor metastasis. |
Author | Kim, Seung-Hoon Shin, Hyun Mu Kim, Hang-Rae Lee, Da-Hye Jeong, Han-Seok Cho, Chung-Hyun Lee, Chang-Han |
Author_xml | – sequence: 1 givenname: Han-Seok surname: Jeong fullname: Jeong, Han-Seok organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Pharmacology, College of Medicine, Seoul National University – sequence: 2 givenname: Da-Hye surname: Lee fullname: Lee, Da-Hye organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Pharmacology, College of Medicine, Seoul National University – sequence: 3 givenname: Seung-Hoon surname: Kim fullname: Kim, Seung-Hoon organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Pharmacology, College of Medicine, Seoul National University – sequence: 4 givenname: Chang-Han surname: Lee fullname: Lee, Chang-Han organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Pharmacology, College of Medicine, Seoul National University – sequence: 5 givenname: Hyun Mu orcidid: 0000-0002-4521-8391 surname: Shin fullname: Shin, Hyun Mu organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Wide River Institute of Immunology, College of Medicine, Seoul National University – sequence: 6 givenname: Hang-Rae orcidid: 0000-0002-3983-6193 surname: Kim fullname: Kim, Hang-Rae organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Anatomy and Cell Biology, Seoul National University – sequence: 7 givenname: Chung-Hyun orcidid: 0000-0002-0585-713X surname: Cho fullname: Cho, Chung-Hyun email: iamhyun@snu.ac.kr organization: Department of Biomedical Sciences, College of Medicine, Seoul National University, Department of Pharmacology, College of Medicine, Seoul National University, Ischemic/Hypoxic Disease Institute, College of Medicine, Seoul National University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35094008$$D View this record in MEDLINE/PubMed |
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Snippet | Diabetes mellitus (DM) characterized by hyperglycemia is a chronic metabolic disorder that leads to many symptoms and vascular complications. Despite the close... |
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SubjectTerms | 13/51 13/89 14/34 14/63 38/91 631/67/327 631/80/79/750 64/60 82/51 Animal models Animals Apoptosis Carcinoma, Lewis Lung - genetics Cell Biology Cell migration Diabetes Diabetes mellitus Diabetes Mellitus - metabolism Disease Models, Animal Endothelial cells Endothelial Cells - metabolism GATA-1 protein GATA1 Transcription Factor - metabolism Gene expression Human Genetics Humans Hyperglycemia Hyperglycemia - complications Hyperglycemia - metabolism Internal Medicine Intravenous administration Lung carcinoma Lung Neoplasms - metabolism Medicine Medicine & Public Health Melanoma Metabolic disorders Metastases Metastasis Mice Oncology Oxidative Stress Streptozocin Therapeutic targets Transcription factors Tumor cells |
Title | Hyperglycemia-induced oxidative stress promotes tumor metastasis by upregulating vWF expression in endothelial cells through the transcription factor GATA1 |
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