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旋磁场对人前列腺腺癌细胞的影响。

Effect of gyromagnetic fields on human prostatic adenocarcinoma cells.

作者信息

Lei Hongen, Xu Yongde, Guan Ruili, Li Meng, Hui Yu, Gao Zhezhu, Yang Bicheng, Xin Zhongcheng

机构信息

Andrology Center, Peking University First Hospital, Peking University, Beijing, People's Republic of China.

Department of Urology, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.

出版信息

Onco Targets Ther. 2015 Nov 24;8:3489-97. doi: 10.2147/OTT.S95306. eCollection 2015.

Abstract

PURPOSE

To investigate the biological effect of gyromagnetic fields (GMFs) on cell proliferation and apoptosis of human prostatic adenocarcinoma cells and explore the underlying mechanisms.

METHODS

PC-3 cells were grouped into normal control (NC) and GMF treatment groups. Cell proliferation was analyzed with kit-8 and Ki67 immunofluorescence staining, while cell apoptosis was analyzed with flow cytometry double staining of Annexin V-PE/7-AAD. The Akt and p38 MAPK/Caspase signaling pathways were analyzed by western blotting and immunofluorescence staining, and cell polarization was analyzed with PARD3.

RESULTS

Cell proliferation and activity of the Akt pathway were significantly decreased by the GMF, while cell apoptosis, activity of p38 MAPK, and PARD3-positive cell number were significantly increased in the GMF group compared to the NC group.

CONCLUSION

GMFs inhibit cell proliferation, induce apoptosis, and regulate tumor cell polarity conditions, potentially through down-regulating Akt, activating the p38 MAPK/Caspase pathway, and promoting PARD3 expression in PC-3 cells.

摘要

目的

研究旋磁波(GMFs)对人前列腺腺癌细胞增殖和凋亡的生物学效应,并探讨其潜在机制。

方法

将PC-3细胞分为正常对照组(NC)和GMF处理组。采用试剂盒-8和Ki67免疫荧光染色分析细胞增殖,采用Annexin V-PE/7-AAD流式细胞术双染分析细胞凋亡。通过蛋白质免疫印迹法和免疫荧光染色分析Akt和p38丝裂原活化蛋白激酶/半胱天冬酶信号通路,并用PARD3分析细胞极化。

结果

与NC组相比,GMF组细胞增殖和Akt信号通路活性显著降低,而细胞凋亡、p38丝裂原活化蛋白激酶活性和PARD3阳性细胞数显著增加。

结论

GMFs可能通过下调Akt、激活p38丝裂原活化蛋白激酶/半胱天冬酶通路和促进PC-3细胞中PARD3表达来抑制细胞增殖、诱导凋亡并调节肿瘤细胞极性状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e720/4664505/e5078c7b82bf/ott-8-3489Fig1.jpg

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