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PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis

Objectives: This study aims to investigate the function of the protein arginine methyltransferase 5 (PRMT5) and fibroblast growth factor receptor 3 (FGFR3)/Akt signaling axis in the epithelial-mesenchymal transition (EMT) of human lung cancer. Methods: The mRNA and protein expression levels of PRMT5...

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Autores principales: Zheng, Yonghua, Lu, Jingjing, Hu, Xiaoyan, Hu, Xiaobiao, Gao, Xiwen, Zhou, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026111/
https://www.ncbi.nlm.nih.gov/pubmed/36927233
http://dx.doi.org/10.1177/15330338231161139
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author Zheng, Yonghua
Lu, Jingjing
Hu, Xiaoyan
Hu, Xiaobiao
Gao, Xiwen
Zhou, Jie
author_facet Zheng, Yonghua
Lu, Jingjing
Hu, Xiaoyan
Hu, Xiaobiao
Gao, Xiwen
Zhou, Jie
author_sort Zheng, Yonghua
collection PubMed
description Objectives: This study aims to investigate the function of the protein arginine methyltransferase 5 (PRMT5) and fibroblast growth factor receptor 3 (FGFR3)/Akt signaling axis in the epithelial-mesenchymal transition (EMT) of human lung cancer. Methods: The mRNA and protein expression levels of PRMT5, FGFR3, p-Akt, and EMT markers are determined by quantitative real-time PCR and Western blotting, respectively; the expression and localization of PRMT5, p-Akt, and proliferating cell nuclear antigen are detected by immunofluorescence; the human lung cancer cell proliferation is measured by MTS assay. Results: PRMT5 and FGFR3 are highly expressed in human lung cancer tissues and are closely related to lymphatic metastasis. Moreover, down-regulation of PRMT5 by lentivirus-mediated shRNAs or inhibition of PRMT5 by specific inhibitors attenuates FGFR3 expression, Akt phosphorylation, and lung cancer cell proliferation. Further studies show that silencing PRMT5 impairs EMT-related markers, including vimentin, collagen I, and β-catenin. Conversely, ectopic expression of PRMT5 increases FGFR3 expression, Akt phosphorylation, and EMT-related markers, suggesting that PRMT5 regulates metastasis probably through the FGFR3/Akt signaling axis. Conclusion: PRMT5/FGFR3/Akt signaling axis controls human lung cancer progression and metastasis and also implies that PRMT5 may serve as a prognostic biomarker and therapeutic candidate for treating lung cancer.
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spelling pubmed-100261112023-03-21 PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis Zheng, Yonghua Lu, Jingjing Hu, Xiaoyan Hu, Xiaobiao Gao, Xiwen Zhou, Jie Technol Cancer Res Treat Original Article Objectives: This study aims to investigate the function of the protein arginine methyltransferase 5 (PRMT5) and fibroblast growth factor receptor 3 (FGFR3)/Akt signaling axis in the epithelial-mesenchymal transition (EMT) of human lung cancer. Methods: The mRNA and protein expression levels of PRMT5, FGFR3, p-Akt, and EMT markers are determined by quantitative real-time PCR and Western blotting, respectively; the expression and localization of PRMT5, p-Akt, and proliferating cell nuclear antigen are detected by immunofluorescence; the human lung cancer cell proliferation is measured by MTS assay. Results: PRMT5 and FGFR3 are highly expressed in human lung cancer tissues and are closely related to lymphatic metastasis. Moreover, down-regulation of PRMT5 by lentivirus-mediated shRNAs or inhibition of PRMT5 by specific inhibitors attenuates FGFR3 expression, Akt phosphorylation, and lung cancer cell proliferation. Further studies show that silencing PRMT5 impairs EMT-related markers, including vimentin, collagen I, and β-catenin. Conversely, ectopic expression of PRMT5 increases FGFR3 expression, Akt phosphorylation, and EMT-related markers, suggesting that PRMT5 regulates metastasis probably through the FGFR3/Akt signaling axis. Conclusion: PRMT5/FGFR3/Akt signaling axis controls human lung cancer progression and metastasis and also implies that PRMT5 may serve as a prognostic biomarker and therapeutic candidate for treating lung cancer. SAGE Publications 2023-03-17 /pmc/articles/PMC10026111/ /pubmed/36927233 http://dx.doi.org/10.1177/15330338231161139 Text en © The Author(s) 2023 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 page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Article
Zheng, Yonghua
Lu, Jingjing
Hu, Xiaoyan
Hu, Xiaobiao
Gao, Xiwen
Zhou, Jie
PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title_full PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title_fullStr PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title_full_unstemmed PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title_short PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis
title_sort prmt5/fgfr3/akt signaling axis facilitates lung cancer cell metastasis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026111/
https://www.ncbi.nlm.nih.gov/pubmed/36927233
http://dx.doi.org/10.1177/15330338231161139
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