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PRMT7 介导的 SHANK2 精氨酸甲基化通过激活内体 FAK 信号促进人乳腺癌转移。

Arginine methylation of SHANK2 by PRMT7 promotes human breast cancer metastasis through activating endosomal FAK signalling.

机构信息

The Key Laboratory of Molecular Epigenetics of the Ministry of Education, Northeast Normal University, Changchun, China.

The Institute of Genetics and Cytology, Northeast Normal University, Changchun, China.

出版信息

Elife. 2020 Aug 26;9:e57617. doi: 10.7554/eLife.57617.

DOI:10.7554/eLife.57617
PMID:32844749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7494359/
Abstract

Arginine methyltransferase PRMT7 is associated with human breast cancer metastasis. Endosomal FAK signalling is critical for cancer cell migration. Here we identified the pivotal roles of PRMT7 in promoting endosomal FAK signalling activation during breast cancer metastasis. PRMT7 exerted its functions through binding to scaffold protein SHANK2 and catalyzing di-methylation of SHANK2 at R240. SHANK2 R240 methylation exposed ANK domain by disrupting its SPN-ANK domain blockade, promoting in co-accumulation of dynamin2, talin, FAK, cortactin with SHANK2 on endosomes. In addition, SHANK2 R240 methylation activated endosomal FAK/cortactin signals in vitro and in vivo. Consistently, all the levels of PRMT7, methylated SHANK2, FAK Y397 phosphorylation and cortactin Y421 phosphorylation were correlated with aggressive clinical breast cancer tissues. These findings characterize the PRMT7-dependent SHANK2 methylation as a key player in mediating endosomal FAK signals activation, also point to the value of SHANK2 R240 methylation as a target for breast cancer metastasis.

摘要

精氨酸甲基转移酶 PRMT7 与人类乳腺癌转移有关。内体 FAK 信号对于癌细胞迁移至关重要。在这里，我们确定了 PRMT7 在促进乳腺癌转移过程中内体 FAK 信号激活中的关键作用。PRMT7 通过与支架蛋白 SHANK2 结合并催化 SHANK2 在 R240 处的二甲基化来发挥其功能。SHANK2 R240 甲基化通过破坏其 SPN-ANK 结构域阻断来暴露 ANK 结构域，促进 dynamin2、talin、FAK、cortactin 与内体上的 SHANK2 共积累。此外，SHANK2 R240 甲基化在体外和体内激活了内体 FAK/cortactin 信号。一致地，PRMT7、甲基化的 SHANK2、FAK Y397 磷酸化和 cortactin Y421 磷酸化的所有水平都与侵袭性临床乳腺癌组织相关。这些发现将 PRMT7 依赖性 SHANK2 甲基化描述为介导内体 FAK 信号激活的关键因素，也表明 SHANK2 R240 甲基化作为乳腺癌转移的靶点具有价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/28b6d03df913/elife-57617-fig9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/28b6d03df913/elife-57617-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/33d4d70127bb/elife-57617-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/7409cc873346/elife-57617-fig1-figsupp1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/79daf934957b/elife-57617-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/c4587537d568/elife-57617-fig6-figsupp1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8165/7494359/28b6d03df913/elife-57617-fig9.jpg

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