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BRMS1介导的转移抑制及miR-31替代疗法对claudin低表达细胞系的作用

Metastasis inhibition by BRMS1 and miR-31 replacement therapy in claudin-low cell lines.

作者信息

Farokhimanesh Samila, Forouzandeh Moghadam Mehdi, Ebrahimi Marzieh

机构信息

Department of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

Department of Biotechnology, Science and Research Branch, Islamic Azad Unversity, Tehran, Iran.

出版信息

Iran J Basic Med Sci. 2020 Feb;23(2):264-270. doi: 10.22038/IJBMS.2019.35674.8500.

DOI:10.22038/IJBMS.2019.35674.8500
PMID:32405371
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7211348/
Abstract

OBJECTIVES

The growing trend of research demonstrates that dynamic expression of two metastasis repressor classes (metastasis suppressor genes and anti-metastatic miRNA) has a close relationship with tumor invasion and metastasis. Using different strategies, it was revealed that cellular levels of miR-31 and Breast cancer Metastasis Suppressor1 (BRMS1) protein, which are among the most significant modulators of metastasis, have a correlation with the cell's capability for invading and metastasizing; cells containing higher levels of miR-31 or BRMS1 were less metastatic. This project was carried out to determine whether the combinations of miR-31 and BRMS1 genes are able to enhance the capability of repressing the claudin-low breast cancer cell (MDA-MB-231) invasion.

MATERIALS AND METHODS

This study used a restoration-based approach by miR-31 mimic and optimized BRMS1 gene sequences, which were cloned into a chimeric construct and transfected to the MDA-M231cells.

RESULTS

Our data revealed that the simultaneous expression of anti-metastasis miR and metastasis suppressor might inhibit migration and invasion in MDA-MB-231 cells efficiently.

CONCLUSION

This combinatorial use of anti-metastatic miR and gene suggests a new therapeutic intervention for metastasis inhibition in MDA-MB-231.

摘要

目的

越来越多的研究趋势表明,两类转移抑制因子(转移抑制基因和抗转移miRNA)的动态表达与肿瘤侵袭和转移密切相关。通过不同策略发现,作为转移最重要调节因子之一的miR-31和乳腺癌转移抑制因子1(BRMS1)蛋白的细胞水平与细胞的侵袭和转移能力相关;miR-31或BRMS1水平较高的细胞转移能力较低。开展本项目以确定miR-31和BRMS1基因的组合是否能够增强抑制claudin-low乳腺癌细胞(MDA-MB-231)侵袭的能力。

材料与方法

本研究采用基于miR-31模拟物和优化的BRMS1基因序列的恢复方法,将其克隆到嵌合构建体中并转染至MDA-M231细胞。

结果

我们的数据显示,抗转移miR和转移抑制因子的同时表达可能有效抑制MDA-MB-231细胞的迁移和侵袭。

结论

这种抗转移miR和基因的联合应用为MDA-MB-231的转移抑制提供了一种新的治疗干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/7d771aec0242/IJBMS-23-264-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/ca42b14ac427/IJBMS-23-264-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/d29c577315f5/IJBMS-23-264-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/27feea76397e/IJBMS-23-264-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/3775a68e5c97/IJBMS-23-264-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/7d771aec0242/IJBMS-23-264-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/ca42b14ac427/IJBMS-23-264-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/d29c577315f5/IJBMS-23-264-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/27feea76397e/IJBMS-23-264-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/3775a68e5c97/IJBMS-23-264-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a36/7211348/7d771aec0242/IJBMS-23-264-g005.jpg

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本文引用的文献

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Breast Cancer. 2019 Mar;26(2):215-228. doi: 10.1007/s12282-018-0915-z. Epub 2018 Oct 3.
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Inhibition of breast cancer metastasis by co-transfection of miR-31/193b-mimics.通过共转染miR-31/193b模拟物抑制乳腺癌转移。
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