2023年12月14日发(作者：春半青)
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
翟丽敏;杨硕;李文通
【期刊名称】《临床与实验病理学杂志》
【年(卷),期】2015(000)009
【摘 要】目的：探讨miR-199a-5p对乳腺癌MDA-MB-231细胞的侵袭影响及其作用机制。方法转染miR-199a-5p mimic至MDA-MB-231细胞,Transwell侵袭实验检测miR-199a-5p对MDA-MB-231细胞侵袭能力的影响。采用细胞免疫荧光、Western blot法检测上皮细胞-间充质转化( epithelial-mesenchymal
transition, EMT)分子标志物 E-cadherin、vimentin 的表达。应用Western blot法检测miR-199a-5p mimic及其LNA-siRNA对ERK5、pERK5、EGF、SP1表达的影响。染色体免疫共沉淀( chroma-tin immunoprecipitation, CHIP)技术检测SP1是否与ERK5启动子区结合。结果 miR-199a-5p能抑制MDA-MB-231细胞的侵袭,降低vimentin的表达,增强E-cadherin的表达。同时,miR-199a-5p降低ERK5表达并抑制其磷酸化；EGF、SP1的表达也相应减少。相反,应用LNA-siRNA抑制miR-199a-5p后,ERK5、pERK5、EGF、SP1的表达上调。 CHIP结果显示SP1能与ERK5启动子区结合。结论 miR-199a-5p通过调节EGF、SP1下调ERK5的表达并抑制其磷酸化,进而发挥对乳腺癌MDA-MB-231细胞侵袭的抑制作用。%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.
【总页数】5页(P981-985)
【作 者】翟丽敏;杨硕;李文通
【作者单位】潍坊医学院病理学教研室，潍坊 261053;潍坊医学院病理学教研室，潍坊 261053;潍坊医学院病理学教研室，潍坊 261053
【正文语种】中 文
【中图分类】R737.9
【相关文献】 NA-106a促进乳腺癌MDA-MB-231细胞侵袭的机制研究 [J], 刘志平;岳梦琳
2.没食子酸乙酯对人乳腺癌MDA-MB-231细胞侵袭能力及其作用机制研究 [J],
黄丽英;陈夏
3.氯化锂抑制乳腺癌MDA-MB-231细胞侵袭的机制研究 [J], 王立洪;李庆华;王建;高伟;蔺亚妮;李华文;金薇娜;常国强;庞天翔
沉默Smad4对奥沙利铂抑制乳腺癌MDA-MB-231细胞侵袭和迁移的影响 [J], 马琳艳;宋乐乐;黄莹莹;孙小锦;董淑英;蒋志文;刘浩
5.黄芩素对乳腺癌MDA-MB-231细胞侵袭转移的影响及其相关机制 [J], 裴晓东;孙占勇;陈世军
因版权原因，仅展示原文概要，查看原文内容请购买
2023年12月14日发(作者：春半青)
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
翟丽敏;杨硕;李文通
【期刊名称】《临床与实验病理学杂志》
【年(卷),期】2015(000)009
【摘 要】目的：探讨miR-199a-5p对乳腺癌MDA-MB-231细胞的侵袭影响及其作用机制。方法转染miR-199a-5p mimic至MDA-MB-231细胞,Transwell侵袭实验检测miR-199a-5p对MDA-MB-231细胞侵袭能力的影响。采用细胞免疫荧光、Western blot法检测上皮细胞-间充质转化( epithelial-mesenchymal
transition, EMT)分子标志物 E-cadherin、vimentin 的表达。应用Western blot法检测miR-199a-5p mimic及其LNA-siRNA对ERK5、pERK5、EGF、SP1表达的影响。染色体免疫共沉淀( chroma-tin immunoprecipitation, CHIP)技术检测SP1是否与ERK5启动子区结合。结果 miR-199a-5p能抑制MDA-MB-231细胞的侵袭,降低vimentin的表达,增强E-cadherin的表达。同时,miR-199a-5p降低ERK5表达并抑制其磷酸化；EGF、SP1的表达也相应减少。相反,应用LNA-siRNA抑制miR-199a-5p后,ERK5、pERK5、EGF、SP1的表达上调。 CHIP结果显示SP1能与ERK5启动子区结合。结论 miR-199a-5p通过调节EGF、SP1下调ERK5的表达并抑制其磷酸化,进而发挥对乳腺癌MDA-MB-231细胞侵袭的抑制作用。%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.
【总页数】5页(P981-985)
【作 者】翟丽敏;杨硕;李文通
【作者单位】潍坊医学院病理学教研室，潍坊 261053;潍坊医学院病理学教研室，潍坊 261053;潍坊医学院病理学教研室，潍坊 261053
【正文语种】中 文
【中图分类】R737.9
【相关文献】 NA-106a促进乳腺癌MDA-MB-231细胞侵袭的机制研究 [J], 刘志平;岳梦琳
2.没食子酸乙酯对人乳腺癌MDA-MB-231细胞侵袭能力及其作用机制研究 [J],
黄丽英;陈夏
3.氯化锂抑制乳腺癌MDA-MB-231细胞侵袭的机制研究 [J], 王立洪;李庆华;王建;高伟;蔺亚妮;李华文;金薇娜;常国强;庞天翔
沉默Smad4对奥沙利铂抑制乳腺癌MDA-MB-231细胞侵袭和迁移的影响 [J], 马琳艳;宋乐乐;黄莹莹;孙小锦;董淑英;蒋志文;刘浩
5.黄芩素对乳腺癌MDA-MB-231细胞侵袭转移的影响及其相关机制 [J], 裴晓东;孙占勇;陈世军
因版权原因，仅展示原文概要，查看原文内容请购买