Long noncoding RNA GAS5 impairs the proliferation and invasion of endometrial carcinoma induced by high glucose via targeting miR-222-3p/p27

被引:3
|
作者
Li, Zhenjin [1 ,3 ]
Yu, Zhiqiang [2 ]
Meng, Xuying [3 ]
Zhou, Saijun [3 ]
Xiao, Shumin [3 ]
Li, Xin [3 ]
Liu, Shuaihui [3 ]
Yu, Pei [3 ]
机构
[1] Tianjin Med Univ, Hosp 2, Dept Endocrinol, Tianjin 300211, Peoples R China
[2] Tianjin Cent Hosp Gynecol & Obstet, Dept Anesthesiol, Tianjin 300052, Peoples R China
[3] Tianjin Med Univ, Key Lab Hormone & Dev, Tianjin Key Lab Metab Dis, Metab Dis Hosp,Minist Hlth,Dept Diabet Nephropath, Tianjin 300070, Peoples R China
来源
关键词
Endometrial carcinoma; GAS5; high glucose; miR-222-3p; p27; DIABETES-MELLITUS; CANCER; EXPRESSION; CELLS; P27;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long noncoding RNAs (lncRNAs) have been identified to be critical functional regulator in the human tumors, while the deepgoing mechanism by which lncRNAs modulates the endometrial carcinoma is still elusive. In this work, we found that lncRNA GAS5 was under-expressed in the endometrial carcinoma tissue specimens, especially these samples with type 2 diabetes mellitus. Besides, the aberrant under-expression of GAS5 was correlated with the advanced tumor stage as well as poor prognosis outcome. In cellular experiments, GAS5 was decreased in the cells exposed to the high glucose. Enforced GAS5 expression repressed the tumor phenotype of endometrial carcinoma cells, including proliferation and invasion. Molecular mechanism study further demonstrated that GAS5 functioned as a sponge for miR-222-3p, abrogating its ability of inhibiting p27 protein expression. In conclusion, these results confirmed the vital regulation of GAS5/miR-222-3p/p27 axis in the endometrial carcinoma tumorigenesis.
引用
收藏
页码:2413 / 2421
页数:9
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