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OIP5-AS1/miR-137/ZNF217轴促进上皮性卵巢癌的恶性行为。

OIP5-AS1/miR-137/ZNF217 Axis Promotes Malignant Behaviors in Epithelial Ovarian Cancer.

作者信息

Guo Linlin, Chen Jiabao, Liu Dong, Liu Lili

机构信息

Department of Obstetrics and Gynecology, First Affiliated Hospital of Jinzhou Medical University, Jinnzhou, Liaoning, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Aug 3;12:6707-6717. doi: 10.2147/CMAR.S237726. eCollection 2020.

DOI:10.2147/CMAR.S237726
PMID:32801903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7413701/
Abstract

BACKGROUND

Long non-coding RNAs (lncRNAs) have been reported to play crucial regulatory roles in cellular activities and are associated with the carcinogenesis of various diseases. OIP5-AS1, as a novel lncRNA, function in epithelial ovarian cancer (EOC) still remains unclear.

MATERIAL AND METHODS

qRT-PCR and Western blot analyses were performed to measure relevant expression, as needed. A series of functional experiments were performed to determine the role of OIP5-AS1 in EOC cells. Luciferase report, RNA pull down and RIP assays were performed to testify the interaction between relevant RNAs.

RESULTS

We found that OIP5-AS1 was significantly overexpressed in EOC. Knockdown of OIP5-AS1 inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process, yet facilitated apoptosis in vitro. OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) to elevate ZNF217 expression through sponging miR-137. Furthermore, miR-137 inhibition and ZNF217 upregulation can reverse the effects of silencing OIP5-AS1 on the cellular activities of ovarian cancer cells. Also, depleted OIP5-AS1 hindered tumor growth and metastasis in vivo.

CONCLUSION

OIP5-AS1 regulated ovarian cancer progression via modulating miR-137/ZNF217 signaling, suggesting that targeting OIP5-AS1 could be conducive to EOC clinical treatment.

摘要

背景

长链非编码RNA(lncRNAs)已被报道在细胞活动中发挥关键调节作用,并与多种疾病的致癌作用相关。OIP5-AS1作为一种新型lncRNA,在上皮性卵巢癌(EOC)中的功能仍不清楚。

材料与方法

根据需要进行qRT-PCR和蛋白质免疫印迹分析以检测相关表达。进行了一系列功能实验以确定OIP5-AS1在EOC细胞中的作用。进行荧光素酶报告、RNA下拉和RNA免疫沉淀实验以证实相关RNA之间的相互作用。

结果

我们发现OIP5-AS1在EOC中显著过表达。敲低OIP5-AS1可抑制细胞增殖、迁移、侵袭和上皮-间质转化(EMT)过程,但在体外促进细胞凋亡。OIP5-AS1作为一种竞争性内源RNA(ceRNA),通过海绵吸附miR-137来提高ZNF217的表达。此外,抑制miR-137和上调ZNF217可逆转沉默OIP5-AS1对卵巢癌细胞细胞活性的影响。而且,耗尽OIP5-AS1会阻碍体内肿瘤的生长和转移。

结论

OIP5-AS1通过调节miR-137/ZNF217信号传导来调控卵巢癌进展,这表明靶向OIP5-AS1可能有利于EOC的临床治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/06a78a168b03/CMAR-12-6707-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/0a2893f5747a/CMAR-12-6707-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/dc264577a531/CMAR-12-6707-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/7d7be0c84fe5/CMAR-12-6707-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/e5c84f3127cc/CMAR-12-6707-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/06a78a168b03/CMAR-12-6707-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/0a2893f5747a/CMAR-12-6707-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/dc264577a531/CMAR-12-6707-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/7d7be0c84fe5/CMAR-12-6707-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/e5c84f3127cc/CMAR-12-6707-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b71/7413701/06a78a168b03/CMAR-12-6707-g0005.jpg

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