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长链非编码RNA USP2-AS1通过海绵吸附miR-520d-3p并上调KIAA1522促进卵巢癌细胞增殖和迁移。

Long Non-Coding RNA USP2-AS1 Accelerates Cell Proliferation and Migration in Ovarian Cancer by Sponging miR-520d-3p and Up-Regulating KIAA1522.

作者信息

Guo Bingqin, Yu Lan, Sun Yanhong, Yao Nan, Ma Li

机构信息

Department of Pathology, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233030, Anhui, People's Republic of China.

Department of Obstetrics and Gynecology, Huangshan People's Hospital of Anhui Province, Huangshan, Anhui 245000, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Oct 23;12:10541-10550. doi: 10.2147/CMAR.S268863. eCollection 2020.

DOI:10.2147/CMAR.S268863
PMID:33122952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7591011/
Abstract

BACKGROUND

Ovarian cancer is one of the malignant tumors attacking the female reproductive system. Currently, increasing studies have clearly determined the importance of long non-coding RNAs (lncRNAs) in various human cancers including ovarian cancer. However, the role and in-depth mechanism of ubiquitin specific peptidase 2 antisense RNA 1 (USP2-AS1) in ovarian cancer have been not reported yet.

PURPOSE

We were absorbed into exploring the character of USP2-AS1 in ovarian cancer.

METHODS

RT-qPCR analysis reflected gene expression. The GEPIA database provided further evidences, and bioinformatics tools analyzed the potential molecules downstream USP2-AS1 in ovarian cancer. The changes on ovarian cancer cellular functions were assessed via EdU, TUNEL, JC-1 and transwell assays. RNA pull down, RIP and luciferase reporter assays estimated molecule interactions.

RESULTS

USP2-AS1 was obviously up-regulated in ovarian cancer tissues and cell lines. Inhibiting USP2-AS1 had anti-proliferation, pro-apoptosis, and anti-migration effects on ovarian cancer cells. Furthermore, we confirmed that USP2-AS1 sequestered miR-520d-3p to enhance KIAA1522. In addition, miR-520d-3p silence reversed the effect of depleted USP2-AS1 on ovarian cancer cellular behaviors, while such reversion was then abolished by KIAA1522 knockdown.

CONCLUSION

USP2-AS1 facilitated ovarian cancer progression via miR-520d-3p/KIAA1522 axis, implying USP2-AS1 as a new perspective for the treatment of ovarian cancer.

摘要

背景

卵巢癌是侵袭女性生殖系统的恶性肿瘤之一。目前，越来越多的研究已明确确定长链非编码RNA（lncRNA）在包括卵巢癌在内的各种人类癌症中的重要性。然而，泛素特异性肽酶2反义RNA 1（USP2-AS1）在卵巢癌中的作用及深入机制尚未见报道。

目的

我们致力于探索USP2-AS1在卵巢癌中的特性。

方法

RT-qPCR分析反映基因表达。GEPIA数据库提供了进一步的证据，生物信息学工具分析了卵巢癌中USP2-AS1下游的潜在分子。通过EdU、TUNEL、JC-1和transwell实验评估卵巢癌细胞功能的变化。RNA下拉、RIP和荧光素酶报告实验评估分子间相互作用。

结果

USP2-AS1在卵巢癌组织和细胞系中明显上调。抑制USP2-AS1对卵巢癌细胞具有抗增殖、促凋亡和抗迁移作用。此外，我们证实USP2-AS1通过隔离miR-520d-3p来增强KIAA1522。此外，miR-520d-3p沉默逆转了USP2-AS1缺失对卵巢癌细胞行为的影响，而这种逆转随后被KIAA1522敲低所消除。

结论

USP2-AS1通过miR-520d-3p/KIAA1522轴促进卵巢癌进展，这意味着USP2-AS1有望成为卵巢癌治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/5b8acddfa968/CMAR-12-10541-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/73e55931b692/CMAR-12-10541-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/cd32cca35427/CMAR-12-10541-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/e807eac47a28/CMAR-12-10541-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/b1336f47a145/CMAR-12-10541-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/5b8acddfa968/CMAR-12-10541-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/73e55931b692/CMAR-12-10541-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/cd32cca35427/CMAR-12-10541-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/e807eac47a28/CMAR-12-10541-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/b1336f47a145/CMAR-12-10541-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3515/7591011/5b8acddfa968/CMAR-12-10541-g0005.jpg

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