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miR-618通过靶向FOXP2抑制前列腺癌的迁移和侵袭。

miR-618 Inhibits Prostate Cancer Migration and Invasion by Targeting FOXP2.

作者信息

Song Xian-Lu, Tang Yao, Lei Xiang-Hui, Zhao Shan-Chao, Wu Zi-Qing

机构信息

Department of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China.

Department of Pathology, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China.

出版信息

J Cancer. 2017 Aug 2;8(13):2501-2510. doi: 10.7150/jca.17407. eCollection 2017.

DOI:10.7150/jca.17407
PMID:28900488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5595080/
Abstract

miRNAs play critical role in the development and progression of prostate cancer. Here we studied the role of miR-618 in prostate cancer migration and invasion. miR-618 was downregulated in metastatic androgen-independent prostate cancer (AIPC), patients with low miR-618 had poor outcome. Overexpression of miR-618 inhibited migration and invasion and induced mesenchymal to epithelial transition (MET). Conversely, knockdown of miR-618 promoted migration and invasion and induced epithelial to mesenchymal transition (EMT). FOXP2 was the direct target of miR-618, and promoted TGF-β expression, inhibition of TGF-β reversed the effect of miR-618 knockdown. We further analyzed the correlation between miR-618 expression and FOXP2 in human prostate cancer tissues, and found there was a negative correlation between miR-618 expression and FOXP2 levels. In conclusion, we found miR-618 inhibited prostate cancer migration and invasion by targeting FOXP2 and inhibiting TGF-β.

摘要

微小RNA（miRNAs）在前列腺癌的发生发展过程中发挥着关键作用。在此，我们研究了miR-618在前列腺癌迁移和侵袭中的作用。在转移性雄激素非依赖性前列腺癌（AIPC）中，miR-618表达下调，miR-618水平低的患者预后较差。miR-618的过表达抑制了迁移和侵袭，并诱导了间充质向上皮转化（MET）。相反，敲低miR-618则促进了迁移和侵袭，并诱导了上皮向间充质转化（EMT）。FOXP2是miR-618的直接靶点，并促进转化生长因子-β（TGF-β）的表达，抑制TGF-β可逆转miR-618敲低的作用。我们进一步分析了人前列腺癌组织中miR-618表达与FOXP2之间的相关性，发现miR-618表达与FOXP2水平呈负相关。总之，我们发现miR-618通过靶向FOXP2并抑制TGF-β来抑制前列腺癌的迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/a7cd385f56b9/jcav08p2501g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/2554bf691071/jcav08p2501g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/6aa237208106/jcav08p2501g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/45db9ab92b12/jcav08p2501g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/0b80c95dfe4b/jcav08p2501g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/bce5becccc4e/jcav08p2501g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/a7cd385f56b9/jcav08p2501g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/2554bf691071/jcav08p2501g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/6aa237208106/jcav08p2501g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/45db9ab92b12/jcav08p2501g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/0b80c95dfe4b/jcav08p2501g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/bce5becccc4e/jcav08p2501g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b30f/5595080/a7cd385f56b9/jcav08p2501g006.jpg

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