MiR-199a inhibits the angiogenic potential of endometrial stromal cells under hypoxia by targeting HIF-1α/VEGF pathway

被引:6
|
作者
Dai, Lan [1 ,2 ]
Lou, Weihua [1 ]
Zhu, Jie [1 ]
Zhou, Xingchen [1 ,2 ]
Di, Wen [1 ,2 ]
机构
[1] Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Dept Obstet & Gynecol, Shanghai 200127, Peoples R China
[2] Focus Construct Subject Shanghai Educ Dept, Shanghai Key Lab Gynecol Oncol, Shanghai, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2015年 / 8卷 / 05期
基金
中国国家自然科学基金;
关键词
Endometriosis; miR-199a; angiogenesis; VEGF-A; HIF-1; alpha; ENDOTHELIAL GROWTH-FACTOR; INDUCIBLE FACTOR-1-ALPHA; ANTIANGIOGENIC THERAPY; FACTOR EXPRESSION; DOWN-REGULATION; FACTOR VEGF; B PATHWAY; CANCER; MICRORNA-199A-5P; INVASIVENESS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We previously reported that miR-199a suppressed the invasiveness of endometrial stromal cells (ESCs) by targeting IkappaB kinase beta (IKK beta). This study was to investigate the role of miR-199a in the angiogenic potential of ESCs under hypoxia. Forced overexpression of miR-199a in ESCs significantly attenuated its angiogenic potential under hypoxia. Moreover, miR-199a down-regulated the expression level of vascular endothelial growth factor-A (VEGF-A) in ESCs under hypoxic conditions. To delineate the mechanism by which miR-199a reduced VEGF-A production, further analysis of the target genes of miR-199a showed that miR-199a targeted both VEGF-A and Hypoxia-inducible factor (HIF)-1 alpha in ESCs. Our findings indicate that miR-199a may attenuate the angiogenic potential of ESCs under hypoxia partly through HIF-1 alpha/VEGF-A pathway suppression. Therefore, miR-199a may play pivotal roles in the pathogenesis of endometriosis and may become a potential therapeutic target of this disease.
引用
收藏
页码:4735 / 4744
页数:10
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