Long Noncoding RNA SCAMP1 Targets miR-137/CXCL12 Axis to Boost Cell Invasion and Angiogenesis in Ovarian Cancer

被引:20
|
作者
Song, Ran [1 ,2 ]
Liu, Zhihui [2 ]
Lu, Lijuan [3 ]
Liu, Fenglin [1 ]
Zhang, Bei [4 ]
机构
[1] Nanjing Univ Chinese Med, XuZhou TCM Hosp, Dept Oncol, Xuzhou, Jiangsu, Peoples R China
[2] Nanjing Univ Chinese Med, Nanjing, Peoples R China
[3] Suzhou Hosp Tradit Chinese Med, Dept Gynecol, Suzhou, Peoples R China
[4] Xuzhou Cent Hosp, Dept Obstet & Gynecol, Xuzhou, Jiangsu, Peoples R China
关键词
SCAMP1; miR-137; CXCL12; ovarian cancer; PROGRESSION; PROMOTES; CARCINOMA; MICRORNAS;
D O I
10.1089/dna.2019.5312
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ovarian cancer (OC) is one of gynecological malignancies that seriously affects women's health. Mounting evidence demonstrated that long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs) play important roles in various biological processes related to the pathogenesis of OC. This research aimed to investigate the regulatory mechanism of lncRNA SCAMP1/miR-137/CXCL12 (C-X-C motif chemokine ligand 12) axis on OC progression. In this study, we found that SCAMP1 was highly expressed in OC cells, which promoted OC cell invasion and angiogenesis. In addition, our research confirmed that SCAMP1 could bind with miR-137, and SCAMP1 sponged miR-137 to accelerate the progression of OC. We also observed that CXCL12 was a downstream target gene for miR-137, and miR-137 targeted CXCL12 to participate in the regulation of OC. Finally, through TCGA database, we found that SCAMP1 (or CXCL12) was upregulated as well as miR-137 was downregulated in OC tissues, and high (or low) level of them was associated with poor prognosis. miR-137 expression was negatively correlated with SCAMP1 (or CXCL12) expression, and SCAMP1 expression was positively correlated with CXCL12 expression in OC. In summary, our study clarified the role of SCAMP1/miR-137/CXCL12 axis in OC, and this finding may provide a potential therapeutic target of OC.
引用
收藏
页码:1041 / 1050
页数:10
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