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PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer
The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molec...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040599/ https://www.ncbi.nlm.nih.gov/pubmed/33829865 http://dx.doi.org/10.1177/09636897211001772 |
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author | Huang, Jianhao Zheng, Yonghua Zheng, Xiao Qian, Bao Yin, Qi Lu, Jingjing Lei, Han |
author_facet | Huang, Jianhao Zheng, Yonghua Zheng, Xiao Qian, Bao Yin, Qi Lu, Jingjing Lei, Han |
author_sort | Huang, Jianhao |
collection | PubMed |
description | The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molecular mechanisms and signaling cascades are entirely unknown. Here, we show that PRMT5 is the ectopic expression in human lung cancer tissues and cell lines. Further study reveals that silencing PRMT5 by lentivirus-mediated shRNA or blocking of PRMT5 by specific inhibitor GSK591 attenuates the expression levels of EMT-related markers in vivo, using the xenograft mouse model. Moreover, our results show that down-regulation of PRMT5 impairs EGFR/Akt signaling cascades in human lung cancer cells, whereas re-expression of PRMT5 recovers those changes, suggesting that PRMT5 regulates EMT probably through EGFR/Akt signaling axis. Altogether, our results demonstrate that PRMT5 serves as a critical oncogenic regulator and promotes EMT in human lung cancer cells. More importantly, our findings also suggest that PRMT5 may be a potential therapeutic candidate for the treatment of human lung cancer. |
format | Online Article Text |
id | pubmed-8040599 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-80405992021-04-21 PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer Huang, Jianhao Zheng, Yonghua Zheng, Xiao Qian, Bao Yin, Qi Lu, Jingjing Lei, Han Cell Transplant Original Article The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molecular mechanisms and signaling cascades are entirely unknown. Here, we show that PRMT5 is the ectopic expression in human lung cancer tissues and cell lines. Further study reveals that silencing PRMT5 by lentivirus-mediated shRNA or blocking of PRMT5 by specific inhibitor GSK591 attenuates the expression levels of EMT-related markers in vivo, using the xenograft mouse model. Moreover, our results show that down-regulation of PRMT5 impairs EGFR/Akt signaling cascades in human lung cancer cells, whereas re-expression of PRMT5 recovers those changes, suggesting that PRMT5 regulates EMT probably through EGFR/Akt signaling axis. Altogether, our results demonstrate that PRMT5 serves as a critical oncogenic regulator and promotes EMT in human lung cancer cells. More importantly, our findings also suggest that PRMT5 may be a potential therapeutic candidate for the treatment of human lung cancer. SAGE Publications 2021-04-08 /pmc/articles/PMC8040599/ /pubmed/33829865 http://dx.doi.org/10.1177/09636897211001772 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Huang, Jianhao Zheng, Yonghua Zheng, Xiao Qian, Bao Yin, Qi Lu, Jingjing Lei, Han PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title | PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title_full | PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title_fullStr | PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title_full_unstemmed | PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title_short | PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer |
title_sort | prmt5 promotes emt through regulating akt activity in human lung cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040599/ https://www.ncbi.nlm.nih.gov/pubmed/33829865 http://dx.doi.org/10.1177/09636897211001772 |
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