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Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis
MicroRNAs (miRNAs) expressed in endothelial cells (ECs) are powerful regulators of angiogenesis, which is essential for tumor growth and metastasis. Here, we demonstrated that miR-22 is preferentially and highly expressed in ECs, while its endothelial level is significantly downregulated in human no...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Gene & Cell Therapy
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8536510/ https://www.ncbi.nlm.nih.gov/pubmed/34729252 http://dx.doi.org/10.1016/j.omtn.2021.10.003 |
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author | Gu, Yuan Pais, Gianni Becker, Vivien Körbel, Christina Ampofo, Emmanuel Ebert, Elke Hohneck, Johannes Ludwig, Nicole Meese, Eckart Bohle, Rainer M. Zhao, Yingjun Menger, Michael D. Laschke, Matthias W. |
author_facet | Gu, Yuan Pais, Gianni Becker, Vivien Körbel, Christina Ampofo, Emmanuel Ebert, Elke Hohneck, Johannes Ludwig, Nicole Meese, Eckart Bohle, Rainer M. Zhao, Yingjun Menger, Michael D. Laschke, Matthias W. |
author_sort | Gu, Yuan |
collection | PubMed |
description | MicroRNAs (miRNAs) expressed in endothelial cells (ECs) are powerful regulators of angiogenesis, which is essential for tumor growth and metastasis. Here, we demonstrated that miR-22 is preferentially and highly expressed in ECs, while its endothelial level is significantly downregulated in human non-small cell lung cancer (NSCLC) tissues when compared to matched nontumor lung tissues. This reduction of endothelial miR-22 is possibly induced by NSCLC cell-secreted interleukin-1β and subsequently activated transcription factor nuclear factor-κB. Endothelial miR-22 functions as a potent angiogenesis inhibitor that inhibits all of the key angiogenic activities of ECs and consequently NSCLC growth through directly targeting sirtuin 1 and fibroblast growth factor receptor 1 in ECs, leading to inactivation of AKT/mammalian target of rapamycin signaling. These findings provide insight into the molecular mechanisms of NSCLC angiogenesis and indicate that endothelial miR-22 represents a potential target for the future antiangiogenic treatment of NSCLC. |
format | Online Article Text |
id | pubmed-8536510 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Society of Gene & Cell Therapy |
record_format | MEDLINE/PubMed |
spelling | pubmed-85365102021-11-01 Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis Gu, Yuan Pais, Gianni Becker, Vivien Körbel, Christina Ampofo, Emmanuel Ebert, Elke Hohneck, Johannes Ludwig, Nicole Meese, Eckart Bohle, Rainer M. Zhao, Yingjun Menger, Michael D. Laschke, Matthias W. Mol Ther Nucleic Acids Original Article MicroRNAs (miRNAs) expressed in endothelial cells (ECs) are powerful regulators of angiogenesis, which is essential for tumor growth and metastasis. Here, we demonstrated that miR-22 is preferentially and highly expressed in ECs, while its endothelial level is significantly downregulated in human non-small cell lung cancer (NSCLC) tissues when compared to matched nontumor lung tissues. This reduction of endothelial miR-22 is possibly induced by NSCLC cell-secreted interleukin-1β and subsequently activated transcription factor nuclear factor-κB. Endothelial miR-22 functions as a potent angiogenesis inhibitor that inhibits all of the key angiogenic activities of ECs and consequently NSCLC growth through directly targeting sirtuin 1 and fibroblast growth factor receptor 1 in ECs, leading to inactivation of AKT/mammalian target of rapamycin signaling. These findings provide insight into the molecular mechanisms of NSCLC angiogenesis and indicate that endothelial miR-22 represents a potential target for the future antiangiogenic treatment of NSCLC. American Society of Gene & Cell Therapy 2021-10-08 /pmc/articles/PMC8536510/ /pubmed/34729252 http://dx.doi.org/10.1016/j.omtn.2021.10.003 Text en © 2021 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Gu, Yuan Pais, Gianni Becker, Vivien Körbel, Christina Ampofo, Emmanuel Ebert, Elke Hohneck, Johannes Ludwig, Nicole Meese, Eckart Bohle, Rainer M. Zhao, Yingjun Menger, Michael D. Laschke, Matthias W. Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title | Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title_full | Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title_fullStr | Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title_full_unstemmed | Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title_short | Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis |
title_sort | suppression of endothelial mir-22 mediates non-small cell lung cancer cell-induced angiogenesis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8536510/ https://www.ncbi.nlm.nih.gov/pubmed/34729252 http://dx.doi.org/10.1016/j.omtn.2021.10.003 |
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