临床与实验病理学杂志Issue(9)：981-985,5.DOI:10.13315/j.cnki.cjcep.2015.09.005
miRNA-199 a-5 p通过SP1调节ERK5抑制乳腺癌MDA-MB-231细胞侵袭的机制
miRNA-199 a-5 p inhibit the invasion of MDA-MB-231 cells via regulating ERK5 through SP1
翟丽敏 1杨硕 1李文通1
作者信息
- 1. 潍坊医学院病理学教研室，潍坊 261053
- 折叠
摘要
Abstract
Purpose To study the effect and mechanism of miR-199a-5p on the invasion of breast cancer MDA-MB-231 cells. Meth-ods miR-199a-5p mimic was transfected into MDA-MB-231 cells. Influence of miR-199a-5p on the invasion of MDA-MB-231 cell was displayed by Transwell, the expression of epithelial-mesenchymal transition ( EMT) molecular markers ( E-cadherin, vimentin) regulated by miR-199a-5p was determined using immunofluorescence and Western blot. Western blot was employed to assess the levels of ERK5, pERK5, EGF and SP1 in MDA-MB-231 cells dealt with miR-199a-5p mimic and LNA-siRNA. Chromatin immunoprecipita-tion (CHIP) was applied for displaying the reaction of SP1 with ERK5 promoter. Results miR-199a-5p could inhibit the invasion of MDA-MB-231 cells, decrease the expression of vimentin and enhance E-cadherin. Meanwhile, miR-199a-5p decreased the expression of ERK5 and pERK5, the levels of EGF and SP1 were also downregulated. On the contrary, the levels of EGF, SP1, ERK5 and pERK5 were enhanced by employing LNA-siRNA targeting miR-199a-5p. SP1 could bind with ERK5 promoter. Conclusions miR-199a-5p could reduce the expression of ERK5 and pERK5 through regulating EGF and SP1, which functioning the inhibitory effect on invasion of MDA-MB-231 breast cancer cells.关键词
乳腺肿瘤/miR-199a-5p/ERK5/SP1/侵袭Key words
breast neoplasm/miR-199a-5p/ERK5/SP1/invasion分类
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翟丽敏,杨硕,李文通..miRNA-199 a-5 p通过SP1调节ERK5抑制乳腺癌MDA-MB-231细胞侵袭的机制[J].临床与实验病理学杂志,2015,(9):981-985,5.
