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P2X7介导前列腺癌细胞中由三磷酸腺苷驱动的侵袭性。

P2X7 mediates ATP-driven invasiveness in prostate cancer cells.

作者信息

Qiu Ying, Li Wei-Hua, Zhang Hong-Quan, Liu Yan, Tian Xin-Xia, Fang Wei-Gang

机构信息

Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science Center, Beijing, 100191, China; Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.

Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science Center, Beijing, 100191, China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, 100191, China.

出版信息

PLoS One. 2014 Dec 8;9(12):e114371. doi: 10.1371/journal.pone.0114371. eCollection 2014.

DOI:10.1371/journal.pone.0114371
PMID:25486274
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4259308/
Abstract

The ATP-gated P2X7 has been shown to play an important role in invasiveness and metastasis of some tumors. However, the possible links and underlying mechanisms between P2X7 and prostate cancer have not been elucidated. Here, we demonstrated that P2X7 was highly expressed in some prostate cancer cells. Down-regulation of P2X7 by siRNA significantly attenuated ATP- or BzATP-driven migration and invasion of prostate cancer cells in vitro, and inhibited tumor invasiveness and metastases in nude mice. In addition, silencing of P2X7 remarkably attenuated ATP- or BzATP- driven expression changes of EMT/invasion-related genes Snail, E-cadherin, Claudin-1, IL-8 and MMP-3, and weakened the phosphorylation of PI3K/AKT and ERK1/2 in vitro. Similar effects were observed in nude mice. These data indicate that P2X7 stimulates cell invasion and metastasis in prostate cancer cells via some EMT/invasion-related genes, as well as PI3K/AKT and ERK1/2 signaling pathways. P2X7 could be a promising therapeutic target for prostate cancer.

摘要

已证明三磷酸腺苷（ATP）门控的P2X7在某些肿瘤的侵袭和转移中起重要作用。然而，P2X7与前列腺癌之间可能的联系及潜在机制尚未阐明。在此，我们证明P2X7在某些前列腺癌细胞中高表达。通过小干扰RNA（siRNA）下调P2X7可显著减弱体外ATP或2'-（3'-O-苯甲酰基）-ATP驱动的前列腺癌细胞迁移和侵袭，并抑制裸鼠体内肿瘤的侵袭和转移。此外，沉默P2X7可显著减弱体外ATP或2'-（3'-O-苯甲酰基）-ATP驱动的上皮-间质转化（EMT）/侵袭相关基因Snail、E-钙黏蛋白、紧密连接蛋白-1、白细胞介素-8和基质金属蛋白酶-3的表达变化，并减弱PI3K/AKT和ERK1/2的磷酸化。在裸鼠中也观察到类似效应。这些数据表明，P2X7通过一些EMT/侵袭相关基因以及PI3K/AKT和ERK1/2信号通路刺激前列腺癌细胞的侵袭和转移。P2X7可能是前列腺癌一个有前景的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/6cd1f6c4acbe/pone.0114371.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/9964b41e4a6c/pone.0114371.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/4dd106b31a0f/pone.0114371.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/3c7263fb550a/pone.0114371.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/fa61b2ffc808/pone.0114371.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/1cf4195ebcf4/pone.0114371.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/5073a073051a/pone.0114371.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/6cd1f6c4acbe/pone.0114371.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/9964b41e4a6c/pone.0114371.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/8b0c920144a2/pone.0114371.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/4dd106b31a0f/pone.0114371.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/3c7263fb550a/pone.0114371.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/fa61b2ffc808/pone.0114371.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/1cf4195ebcf4/pone.0114371.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/5073a073051a/pone.0114371.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb41/4259308/6cd1f6c4acbe/pone.0114371.g008.jpg

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