Article Summary
王圣坦,朱根海,洪 澜,吴秀容,纪 武.miR-181a通过调控上皮间质转化过程影响卵巢癌细胞的迁移和侵袭[J].现代生物医学进展英文版,2018,(18):3445-3449.
miR-181a通过调控上皮间质转化过程影响卵巢癌细胞的迁移和侵袭
miR-181a Affects Ovarian Cancer Cell Migration and Invasion by Regulating Epithelial-mesenchymal Transition
Received:March 08, 2018  Revised:March 31, 2018
DOI:10.13241/j.cnki.pmb.2018.18.09
中文关键词: miR-181a  卵巢癌  上皮间质转化
英文关键词: miR-181a  Ovarian cancer  EMT
基金项目:海南省科学技术研究与发展计划项目(817316)
Author NameAffiliationE-mail
王圣坦 海南省人民医院妇科 海南 海口 570311 shaochunxia01@tom.com 
朱根海 海南省人民医院妇科 海南 海口 570311  
洪 澜 海南省人民医院妇科 海南 海口 570311  
吴秀容 海南省人民医院妇科 海南 海口 570311  
纪 武 海南省人民医院妇科 海南 海口 570311  
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中文摘要:
      摘要 目的:探讨miR-181a在卵巢癌细胞中的表达及对卵巢癌细胞的迁移和侵袭的影响和可能机制。方法:采用细胞免疫荧光检测卵巢癌细胞中抗波形蛋白和E-钙粘蛋白的表达,Western blotting检测miR-181a对抗波形蛋白和E-钙粘蛋白的表达情况的调控;划痕愈合实验检测miR-181a对卵巢癌细胞迁移能力的影响;Transwell侵袭实验检测miR-181a对卵巢癌细胞侵袭能力的影响。结果:增加miR-181a的表达后,EMT过程中的相关蛋白激活水平下调,miR-181a一定程度上可以抑制卵巢癌细胞的EMT过程;过表达miR-181a后可以明显影响Vimentin[D1(4.58±0.85)vs(0.29±0.02),P<0.05;D5(4.16±0.79)vs(0.29±0.02),P<0.05]和E-Cadherin[D1(4.75±0.41) vs. (4.56±0.38),P>0.05;D5(2.19±0.18) vs. (4.56±0.38),P<0.05]蛋白的表达;COC1细胞的迁移能力随miR-181a的表达的增高而降低[(19.24±4.31)% vs. (25.95±6.02)%,P<0.05;(51.25±8.75)% vs. (73.49±12.54)%,P<0.05];过表达miR-181a后可以一定程度上减弱卵巢癌COC1细胞的侵袭能力[(74.64±8.21)vs(231.98±21.72),P<0.05]。结论:miR-181a通过调控上皮间质转化过程影响卵巢癌细胞的迁移和侵袭行为。
英文摘要:
      ABSTRACT Objective: To investigate the effect of miR-181a on the migration and invasion of ovarian cancer cells by regulating the process of epithelial mesenchymal transition and its mechanism. Methods: Immunofluorescence was used to detect the expression of anti-vimentin and E - cadherin in ovarian cancer cells. Western blotting was used to detect the expression of miR-181a against vimentin and E-cadherin. The effect of miR-181a on the migration ability of ovarian cancer cells was examined by the method of scratch healing. Transwell invasion assay was used to detect the effect of miR-181a on the invasive ability of ovarian cancer cells. Results: After miR-181a was increased, the activation of related proteins in EMT was down-regulated, and miR-181a could inhibit the EMT of ovarian cancer cells to a certain extent. Overexpression of miR-181a could significantly affect Vimentin [D1 (4.58±0.85) (P<0.05) and E-Cad- herin [D1 (4.75±0.41) vs. (4.56±0.38) vs P>0.05 (P<0.05) (19.24±4.31)% vs. (25.95±0.05), respectively; D5 (2.19±0.18) vs. (4.56 ±0.38), P<0.05]. The migration ability of COC1 cells decreased with the increase of miR- (51.25±8.75)% vs. (73.49±12.54)%, P<0.05]. Overexpression of miR-181a attenuated the invasiveness of ovarian cancer COC1 cells to a certain degree [(74.64±8.21) vs (231.98±21.72), P<0.05]. Conclusion: miR-181a affects the migration and invasion of ovarian cancer cells by regulating the process of epithelial mesenchymal transition.
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