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Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin
Angiogenesis is closely associated with tumorigenesis, invasion, and metastasis by providing oxygen and nutrients. Recently, increasing evidence indicates that cancer‐derived exosomes which contain proteins, coding, and noncoding RNAs (ncRNAs) were shown to have proangiogenic function in cancer. A 2...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8088954/ https://www.ncbi.nlm.nih.gov/pubmed/33205567 http://dx.doi.org/10.1111/cas.14740 |
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author | Chen, Xiaocui Zhang, Shuqiong Du, Kun Zheng, Naisheng Liu, Yi Chen, Hui Xie, Guohua Ma, Yanhui Zhou, Yunlan Zheng, Yingxia Zeng, Lingfang Yang, Junyao Shen, Lisong |
author_facet | Chen, Xiaocui Zhang, Shuqiong Du, Kun Zheng, Naisheng Liu, Yi Chen, Hui Xie, Guohua Ma, Yanhui Zhou, Yunlan Zheng, Yingxia Zeng, Lingfang Yang, Junyao Shen, Lisong |
author_sort | Chen, Xiaocui |
collection | PubMed |
description | Angiogenesis is closely associated with tumorigenesis, invasion, and metastasis by providing oxygen and nutrients. Recently, increasing evidence indicates that cancer‐derived exosomes which contain proteins, coding, and noncoding RNAs (ncRNAs) were shown to have proangiogenic function in cancer. A 26‐nt‐long ncRNA (X26nt) is generated in the process of inositol‐requiring enzyme 1 alpha (IRE1α)‐induced unspliced XBP1 splicing. However, the role of X26nt in the angiogenesis of gastric cancer (GC) remains largely unknown. In the present study, we found that X26nt was significantly elevated in GC and GC exosomes. Then, we verified that X26nt could be delivered into human umbilical vein endothelial cells (HUVECs) via GC cell exosomes and promote the proliferation, migration, and tube formation of HUVECs. We revealed that exosomal X26nt decreased vascular endothelial cadherin (VE‐cadherin) by directly combining the 3′UTR of VE‐cadherin mRNA in HUVECs, thereby increasing vascular permeability. We further demonstrated that X26nt accelerates the tumor growth and angiogenesis in a mouse subcutaneous tumor model. Our findings investigate a unique intercellular communication mediated by cancer‐derived exosomes and reveal a novel mechanism of exosomal X26nt in the regulation of tumor vasculature. |
format | Online Article Text |
id | pubmed-8088954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-80889542021-05-10 Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin Chen, Xiaocui Zhang, Shuqiong Du, Kun Zheng, Naisheng Liu, Yi Chen, Hui Xie, Guohua Ma, Yanhui Zhou, Yunlan Zheng, Yingxia Zeng, Lingfang Yang, Junyao Shen, Lisong Cancer Sci Original Articles Angiogenesis is closely associated with tumorigenesis, invasion, and metastasis by providing oxygen and nutrients. Recently, increasing evidence indicates that cancer‐derived exosomes which contain proteins, coding, and noncoding RNAs (ncRNAs) were shown to have proangiogenic function in cancer. A 26‐nt‐long ncRNA (X26nt) is generated in the process of inositol‐requiring enzyme 1 alpha (IRE1α)‐induced unspliced XBP1 splicing. However, the role of X26nt in the angiogenesis of gastric cancer (GC) remains largely unknown. In the present study, we found that X26nt was significantly elevated in GC and GC exosomes. Then, we verified that X26nt could be delivered into human umbilical vein endothelial cells (HUVECs) via GC cell exosomes and promote the proliferation, migration, and tube formation of HUVECs. We revealed that exosomal X26nt decreased vascular endothelial cadherin (VE‐cadherin) by directly combining the 3′UTR of VE‐cadherin mRNA in HUVECs, thereby increasing vascular permeability. We further demonstrated that X26nt accelerates the tumor growth and angiogenesis in a mouse subcutaneous tumor model. Our findings investigate a unique intercellular communication mediated by cancer‐derived exosomes and reveal a novel mechanism of exosomal X26nt in the regulation of tumor vasculature. John Wiley and Sons Inc. 2021-03-10 2021-05 /pmc/articles/PMC8088954/ /pubmed/33205567 http://dx.doi.org/10.1111/cas.14740 Text en © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Chen, Xiaocui Zhang, Shuqiong Du, Kun Zheng, Naisheng Liu, Yi Chen, Hui Xie, Guohua Ma, Yanhui Zhou, Yunlan Zheng, Yingxia Zeng, Lingfang Yang, Junyao Shen, Lisong Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title | Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title_full | Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title_fullStr | Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title_full_unstemmed | Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title_short | Gastric cancer–secreted exosomal X26nt increases angiogenesis and vascular permeability by targeting VE‐cadherin |
title_sort | gastric cancer–secreted exosomal x26nt increases angiogenesis and vascular permeability by targeting ve‐cadherin |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8088954/ https://www.ncbi.nlm.nih.gov/pubmed/33205567 http://dx.doi.org/10.1111/cas.14740 |
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