RETRACTED: MicroRNA-218 inhibits proliferation and invasion in ovarian cancer by targeting Runx2 (Retracted Article)

被引:29
作者
Li, Na [1 ]
Wang, Lufei [2 ]
Tan, Guangyun [3 ]
Guo, Zhiheng [1 ]
Liu, Lei [1 ]
Yang, Ming [4 ]
He, Jin [1 ]
机构
[1] Jilin Univ, Dept Gynecol & Obstet, Hosp 1, Changchun 130021, Jilin, Peoples R China
[2] Jilin Univ, Dept Ophthalmol, Hosp 2, Changchun 130022, Jilin, Peoples R China
[3] Jilin Univ, Dept Immunol, Hosp 1, Inst Translat Med, Changchun 130021, Jilin, Peoples R China
[4] Jilin Univ, Dept Breast Surg, Hosp 1, Changchun 130021, Jilin, Peoples R China
关键词
MiR-218; ovarian cancer; RUNX2; proliferation; invasion; TRANSCRIPTION FACTOR RUNX2; DOWN-REGULATION; TUMOR-GROWTH; MIR-218; PROGRESSION; EXPRESSION; CARCINOMA; DIFFERENTIATION; CISPLATIN; REGULATOR;
D O I
10.18632/oncotarget.21069
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNA-218 (miR-218) has been implicated in the development and progression of multiple cancers. We investigated the role of miR-218 in ovarian cancer progression. We found that miR-218 expression levels were lower in ovarian cancer tissues and cell lines than in adjacent normal tissues or a normal ovarian cell line. miR-218 levels associated with International Federation of Gynecology and Obstetrics (FIGO) stage and lymph node metastasis. Exogenous expression of miR-218 inhibited cell proliferation, colony formation, migration, and invasion in vitro and suppressed tumor growth in a tumor-bearing nude mouse model. Runt-related transcription factor 2 (RUNX2) was identified as a direct functional target of miR-218, and its expression was inversely correlated with miR-218 expression in ovarian cancer tissues. RUNX2 overexpression rescued the suppressive effect of miR-218 on ovarian cancer cell proliferation, colony formation, migration, and invasion. These findings highlight an important role played bymiR-218 in the regulation of cancer growth and metastasis, in part by repressing RUNX2, and revealed the potential of miR-218 as a new therapeutic target inovarian cancer.
引用
收藏
页码:91530 / 91541
页数:12
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