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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...

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Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society of Gene & Cell Therapy 2021
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.
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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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