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Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle

Prostate cancer is one of the most common types of cancer affecting men worldwide; however, its etiology and pathological mechanisms remain poorly understood. Mechanical stimulation plays a key role in prostate cancer development. Piezo type mechanosensitive ion channel component 1 (Piezo1), which f...

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Autores principales: Han, Yu, Liu, Chao, Zhang, Dongfang, Men, Hongchao, Huo, Lifang, Geng, Qiaowei, Wang, Shengnan, Gao, Yiting, Zhang, Wei, Zhang, Yongjian, Jia, Zhanfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6685593/
https://www.ncbi.nlm.nih.gov/pubmed/31322184
http://dx.doi.org/10.3892/ijo.2019.4839
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author Han, Yu
Liu, Chao
Zhang, Dongfang
Men, Hongchao
Huo, Lifang
Geng, Qiaowei
Wang, Shengnan
Gao, Yiting
Zhang, Wei
Zhang, Yongjian
Jia, Zhanfeng
author_facet Han, Yu
Liu, Chao
Zhang, Dongfang
Men, Hongchao
Huo, Lifang
Geng, Qiaowei
Wang, Shengnan
Gao, Yiting
Zhang, Wei
Zhang, Yongjian
Jia, Zhanfeng
author_sort Han, Yu
collection PubMed
description Prostate cancer is one of the most common types of cancer affecting men worldwide; however, its etiology and pathological mechanisms remain poorly understood. Mechanical stimulation plays a key role in prostate cancer development. Piezo type mechanosensitive ion channel component 1 (Piezo1), which functions as a cell sensor and transducer of mechanical stimuli, may have a crucial role in the development of prostate cancer. In the present study, the expression of the Piezo1 channel was demonstrated to be significantly elevated in prostate cancer cell lines and in human prostate malignant tumor tissues. Downregulation of Piezo1 significantly suppressed the viability, proliferation and migration of prostate cancer cells in vitro, and inhibited prostate tumor growth in vivo. The activation of the Akt/mTOR pathway or acceleration of cell cycle progression from G(0)/G(1) to S phase may downstream consequences of Piezo 1 signal pathway activation. Downregulation of Piezo1 considerably suppressed Ca(2+) signal increments, inhibited the phosphorylation of Akt and mTOR and arrested the cell cycle of prostate cancer cells at G(0)/G(1) phase in while inhibiting the activation of CDK4 and cyclin D1. Taken together, these findings suggest that Piezo1 channels have a crucial role in prostate cancer development and may, therefore, be a novel therapeutic target in the treatment of prostate cancer.
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spelling pubmed-66855932019-08-15 Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle Han, Yu Liu, Chao Zhang, Dongfang Men, Hongchao Huo, Lifang Geng, Qiaowei Wang, Shengnan Gao, Yiting Zhang, Wei Zhang, Yongjian Jia, Zhanfeng Int J Oncol Articles Prostate cancer is one of the most common types of cancer affecting men worldwide; however, its etiology and pathological mechanisms remain poorly understood. Mechanical stimulation plays a key role in prostate cancer development. Piezo type mechanosensitive ion channel component 1 (Piezo1), which functions as a cell sensor and transducer of mechanical stimuli, may have a crucial role in the development of prostate cancer. In the present study, the expression of the Piezo1 channel was demonstrated to be significantly elevated in prostate cancer cell lines and in human prostate malignant tumor tissues. Downregulation of Piezo1 significantly suppressed the viability, proliferation and migration of prostate cancer cells in vitro, and inhibited prostate tumor growth in vivo. The activation of the Akt/mTOR pathway or acceleration of cell cycle progression from G(0)/G(1) to S phase may downstream consequences of Piezo 1 signal pathway activation. Downregulation of Piezo1 considerably suppressed Ca(2+) signal increments, inhibited the phosphorylation of Akt and mTOR and arrested the cell cycle of prostate cancer cells at G(0)/G(1) phase in while inhibiting the activation of CDK4 and cyclin D1. Taken together, these findings suggest that Piezo1 channels have a crucial role in prostate cancer development and may, therefore, be a novel therapeutic target in the treatment of prostate cancer. D.A. Spandidos 2019-07-15 /pmc/articles/PMC6685593/ /pubmed/31322184 http://dx.doi.org/10.3892/ijo.2019.4839 Text en Copyright: © Han et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Han, Yu
Liu, Chao
Zhang, Dongfang
Men, Hongchao
Huo, Lifang
Geng, Qiaowei
Wang, Shengnan
Gao, Yiting
Zhang, Wei
Zhang, Yongjian
Jia, Zhanfeng
Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title_full Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title_fullStr Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title_full_unstemmed Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title_short Mechanosensitive ion channel Piezo1 promotes prostate cancer development through the activation of the Akt/mTOR pathway and acceleration of cell cycle
title_sort mechanosensitive ion channel piezo1 promotes prostate cancer development through the activation of the akt/mtor pathway and acceleration of cell cycle
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6685593/
https://www.ncbi.nlm.nih.gov/pubmed/31322184
http://dx.doi.org/10.3892/ijo.2019.4839
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