MiR-199a-3p suppresses proliferation and invasion of prostate cancer cells by targeting Smad1.

MiR-199a-3p suppresses proliferation and invasion of prostate cancer cells by targeting Smad1.
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MiR-199a-3p通过靶向Smad1抑制前列腺癌细胞的增殖和侵袭

DOI:
10.18632/oncotarget.17191
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发表时间:
2017-08-08
期刊:
影响因子:
--
通讯作者:
Guo H
Guo H
中科院分区:
其他
文献类型:
--
作者:
Qu F;Zheng J;Gan W;Lian H;He H;Li W;Yuan T;Yang Y;Li X;Ji C;Yan X;Xu L;Guo H

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目的探讨miR-199a-3p和Smad1对前列腺癌(Pca)细胞增殖、迁移和侵袭的影响。结果MIR-199a-3p在PCa组织中的表达明显低于癌旁正常组织(P<0.05)。过表达miR-199a-3p可显著抑制PCa细胞的增殖和侵袭(P<0.05)。MIR-199a-3p与Smad1表达呈负相关,Smad1过表达可拮抗miR-199a-3p对PCa细胞的作用。材料与方法收集54例PCa患者的前列腺癌组织及癌旁正常组织。用实时定量聚合酶链式反应(RT-qPCR)检测组织和细胞中miR-199a-3p和Smad1mRNA的表达,用免疫组织化学方法检测Smad1蛋白的表达。用荧光素酶报告基因分析评价miR-199a-3p与Smad1的靶向关系。将miR-199a-3p模拟物和Smad1-cDNA3基因分别导入PCa细胞系(即PC-3细胞)。用四甲基偶氮唑盐比色法和Transwell法检测PCa细胞的增殖、迁移和侵袭能力。结论MIR-199a-3p通过靶向Smad1抑制PCa细胞的增殖和侵袭。
Objectives This study was intended to analyze effects of miR-199a-3p and Smad1 on proliferation, migration and invasion of prostate cancer (PCa) cells. Results MiR-199a-3p was significantly decreased in PCa tissues in comparison to that in adjacent normal tissues (P < 0.05). Over-expressed miR-199a-3p markedly suppressed proliferation and invasion of PCa cells (P < 0.05). MiR-199a-3p was negatively correlated with Smad1 expression, and overexpression of Smad1 could antagonize the effects of miR-199a-3p on PCa cells. Materials and methods The PCa tissues and their adjacent normal tissues were collected from 54 PCa patients. Expressions of miR-199a-3p and Smad1 mRNA in tissues and cells were evaluated with real-time quantitative polymerase chain reaction (RT-qPCR), and immunohistochemistry assay was used to detect Smad1 protein expressions. The target relationship between miR-199a-3p and Smad1 was assessed by luciferase reporter assay. The PCa cell lines (i.e. PC-3 cells) were transfected with miR-199a-3p mimics and Smad1-cDNA. MTT and Transwell assays were applied to detect proliferative, migratory and invasive abilities of PCa cells. Conclusions MiR-199a-3p suppressed proliferation and invasion of PCa cells by targeting Smad1.
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