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前列腺素 E2 通过激活瞬时受体电位 melastatin 7 通道增加人胶质母细胞瘤细胞的迁移和增殖。

Prostaglandin E2 increases migration and proliferation of human glioblastoma cells by activating transient receptor potential melastatin 7 channels.

机构信息

Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science, Fudan University, Shanghai, China.

出版信息

J Cell Mol Med. 2018 Dec;22(12):6327-6337. doi: 10.1111/jcmm.13931. Epub 2018 Oct 19.

DOI:10.1111/jcmm.13931
PMID:30338939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6237613/
Abstract

Recent studies showed that both prostaglandin E2 (PGE2) and transient receptor potential melastatin 7 (TRPM7) play important roles in migration and proliferation of human glioblastoma cells. In this study, we tested the association between PGE2 and TRPM7. We found that PGE2 increased TRPM7 currents in HEK293 and human glioblastoma A172 cells. The PGE2 EP3 receptor antagonist L-798106 abrogated the PGE2 stimulatory effect, while EP3 agonist 17-phenyl trinor prostaglandin E2 (17-pt-PGE2) mimicked the effect of PEG2 on TRPM7. The TRPM7 phosphotransferase activity-deficient mutation, K1646R had no effect on PGE2 induced increase of TRPM7 currents. Inhibition of protein kinase A (PKA) activity by Rp-cAMP increased TRPM7 currents. TRPM7 PKA phosphorylation site mutation S1269A abolished the PGE2 effect on TRPM7 currents. PGE2 increased both mRNA and membrane protein expression of TRPM7 in A172 cells. Knockdown of TRPM7 by shRNA abrogated the PGE2 stimulated migration and proliferation of A172 cells. Blockage of TRPM7 with 2-aminoethoxydiphenyl borate (2-APB) or NS8593 had a similar effect as TRPM7-shRNA. In conclusion, our results demonstrate that PGE2 activates TRPM7 via EP3/PKA signalling pathway, and that PGE2 enhances migration and proliferation of human glioblastoma cells by up-regulation of the TRPM7 channel.

摘要

最近的研究表明，前列腺素 E2（PGE2）和瞬时受体电位 melastatin 7（TRPM7）在人胶质母细胞瘤细胞的迁移和增殖中都发挥着重要作用。在本研究中，我们测试了 PGE2 和 TRPM7 之间的关联。我们发现 PGE2 增加了 HEK293 和人胶质母细胞瘤 A172 细胞中的 TRPM7 电流。PGE2 EP3 受体拮抗剂 L-798106 阻断了 PGE2 的刺激作用，而 EP3 激动剂 17-苯基三诺 prostaglandin E2（17-pt-PGE2）模拟了 PGE2 对 TRPM7 的作用。TRPM7 磷酸转移酶活性缺陷突变 K1646R 对 PGE2 诱导的 TRPM7 电流增加没有影响。蛋白激酶 A（PKA）活性的抑制 Rp-cAMP 增加了 TRPM7 电流。TRPM7 PKA 磷酸化位点突变 S1269A 消除了 PGE2 对 TRPM7 电流的作用。PGE2 增加了 A172 细胞中 TRPM7 的 mRNA 和膜蛋白表达。通过 shRNA 敲低 TRPM7 消除了 PGE2 刺激的 A172 细胞迁移和增殖。用 2-氨基乙氧基二苯硼酸盐（2-APB）或 NS8593 阻断 TRPM7 具有与 TRPM7-shRNA 相似的效果。总之，我们的结果表明，PGE2 通过 EP3/PKA 信号通路激活 TRPM7，通过上调 TRPM7 通道增强人胶质母细胞瘤细胞的迁移和增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/7c33ede2bd5a/JCMM-22-6327-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/53526b612148/JCMM-22-6327-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/62e209514ff3/JCMM-22-6327-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/346ab4bed53d/JCMM-22-6327-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/d99676d9d970/JCMM-22-6327-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/de46cb749e45/JCMM-22-6327-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/d21df3be217d/JCMM-22-6327-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/7c33ede2bd5a/JCMM-22-6327-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/53526b612148/JCMM-22-6327-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/62e209514ff3/JCMM-22-6327-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/346ab4bed53d/JCMM-22-6327-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/d99676d9d970/JCMM-22-6327-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/de46cb749e45/JCMM-22-6327-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/d21df3be217d/JCMM-22-6327-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bce2/6237613/7c33ede2bd5a/JCMM-22-6327-g007.jpg

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