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Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway

Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migr...

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Autores principales: Zhou, Kecheng, Chen, Jie, Wu, Jiayu, Xu, Yangxinzi, Wu, Qiaoyun, Yue, Jingjing, Song, Yu, Li, Shengcun, Zhou, Peng, Tu, Wenzhan, Yang, Guanhu, Jiang, Songhe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848265/
https://www.ncbi.nlm.nih.gov/pubmed/31122311
http://dx.doi.org/10.3727/096504019X15579146061957
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author Zhou, Kecheng
Chen, Jie
Wu, Jiayu
Xu, Yangxinzi
Wu, Qiaoyun
Yue, Jingjing
Song, Yu
Li, Shengcun
Zhou, Peng
Tu, Wenzhan
Yang, Guanhu
Jiang, Songhe
author_facet Zhou, Kecheng
Chen, Jie
Wu, Jiayu
Xu, Yangxinzi
Wu, Qiaoyun
Yue, Jingjing
Song, Yu
Li, Shengcun
Zhou, Peng
Tu, Wenzhan
Yang, Guanhu
Jiang, Songhe
author_sort Zhou, Kecheng
collection PubMed
description Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migration, and invasion. However, the role of PFN2 in HNSC development and progression remains unclear. The aim of our study was to investigate the role of PFN2 in the development of HNSC and its possible molecular mechanisms. Bioinformatics showed that increased expression of PFN2 in tumors correlated highly with poor prognosis of HNSC patients. Our results indicated that PFN2 was highly expressed in HNSC tissues and in HNSC cell lines. Knockdown of PFN2 inhibited proliferation, invasion, and migration of HNSC cells, while PFN2 overexpression produced the opposite effects. Using a nude mouse xenograft model, we substantiated the tumor-promoting effect of PFN2 on HNSC in vivo. Furthermore, we found that PFN2 downregulation reduced the phosphorylation of Akt and GSK-3β and reduced the expression of β-catenin in HNSC cells. The opposite was observed when PFN2 was overexpressed. Collectively, these results suggest that PFN2 promotes the proliferation and metastasis of HNSC by activating the PI3K/Akt/β-catenin signaling pathway. Although further validation is needed, we speculate that PFN2 plays a crucial role in HNSC and may be a promising therapeutic target and prognostic biomarker.
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spelling pubmed-78482652021-02-16 Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway Zhou, Kecheng Chen, Jie Wu, Jiayu Xu, Yangxinzi Wu, Qiaoyun Yue, Jingjing Song, Yu Li, Shengcun Zhou, Peng Tu, Wenzhan Yang, Guanhu Jiang, Songhe Oncol Res Article Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migration, and invasion. However, the role of PFN2 in HNSC development and progression remains unclear. The aim of our study was to investigate the role of PFN2 in the development of HNSC and its possible molecular mechanisms. Bioinformatics showed that increased expression of PFN2 in tumors correlated highly with poor prognosis of HNSC patients. Our results indicated that PFN2 was highly expressed in HNSC tissues and in HNSC cell lines. Knockdown of PFN2 inhibited proliferation, invasion, and migration of HNSC cells, while PFN2 overexpression produced the opposite effects. Using a nude mouse xenograft model, we substantiated the tumor-promoting effect of PFN2 on HNSC in vivo. Furthermore, we found that PFN2 downregulation reduced the phosphorylation of Akt and GSK-3β and reduced the expression of β-catenin in HNSC cells. The opposite was observed when PFN2 was overexpressed. Collectively, these results suggest that PFN2 promotes the proliferation and metastasis of HNSC by activating the PI3K/Akt/β-catenin signaling pathway. Although further validation is needed, we speculate that PFN2 plays a crucial role in HNSC and may be a promising therapeutic target and prognostic biomarker. Cognizant Communication Corporation 2019-09-23 /pmc/articles/PMC7848265/ /pubmed/31122311 http://dx.doi.org/10.3727/096504019X15579146061957 Text en Copyright © 2019 Cognizant, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License.
spellingShingle Article
Zhou, Kecheng
Chen, Jie
Wu, Jiayu
Xu, Yangxinzi
Wu, Qiaoyun
Yue, Jingjing
Song, Yu
Li, Shengcun
Zhou, Peng
Tu, Wenzhan
Yang, Guanhu
Jiang, Songhe
Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title_full Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title_fullStr Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title_full_unstemmed Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title_short Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
title_sort profilin 2 promotes proliferation and metastasis of head and neck cancer cells by regulating pi3k/akt/β-catenin signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848265/
https://www.ncbi.nlm.nih.gov/pubmed/31122311
http://dx.doi.org/10.3727/096504019X15579146061957
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