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长链非编码 RNA OIP5-AS1 通过上调 ITGA6 抑制 microRNA-92a 来增强卵巢癌细胞的增殖和转移。

Long non-coding RNA OIP5-AS1 suppresses microRNA-92a to augment proliferation and metastasis of ovarian cancer cells through upregulating ITGA6.

机构信息

Gynaecology and Obstetrics Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, No. 32, West Second Section First Ring Rd, Chengdu, 610072, Sichuan, China.

出版信息

J Ovarian Res. 2022 Feb 16;15(1):25. doi: 10.1186/s13048-021-00937-3.

Abstract

OBJECTIVE

Recently, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as essential biomarkers during development of malignancies. This study was performed to study the roles of lncRNA opa-interacting protein 5 antisense transcript 1 (OIP5-AS1) and miR-92a in ovarian cancer (OC).

METHODS

OIP5-AS1, miR-92a and integrin alpha 6 (ITGA6) expression in OC tissues and cells was assessed. The screened OC cells were respectively with OIP5-AS1-, miR-92a- and ITGA6-related vectors or oligonucleotides . The viability, migration, invasion and apoptosis of the cells were determined and the levels of epithelial-mesenchymal transition (EMT)-related proteins were also measured. The interactions between OIP5-AS1 and miR-92a, and between miR-92a and ITGA6 were confirmed.

RESULTS

OIP5-AS1 and ITGA6 were upregulated while miR-92a was downregulated in OC. Inhibited OIP5-AS1 or downregulated ITGA6 or elevated miR-92a repressed EMT, viability, migration and invasion, and promoted apoptosis of OC cells. OIP5-AS1 as a competing endogenous RNA interacted with miR-92a to regulate ITGA6. These effects that induced by silenced OIP5-AS1 could be reversed by miR-92a inhibition while those that induced by up-regulated miR-92a were reduced by restored ITGA6.

CONCLUSION

OIP5-AS1 silencing promoted miR-92a to repress proliferation and metastasis of OC cells through inhibiting ITGA6.

摘要

目的

长链非编码 RNA(lncRNA)和 microRNA(miRNA)最近被鉴定为恶性肿瘤发展过程中的重要生物标志物。本研究旨在研究 lncRNA opa 相互作用蛋白 5 反义转录物 1(OIP5-AS1)和 miR-92a 在卵巢癌(OC)中的作用。

方法

评估 OIP5-AS1、miR-92a 和整合素 alpha 6(ITGA6)在 OC 组织和细胞中的表达。筛选出的 OC 细胞分别用 OIP5-AS1、miR-92a 和 ITGA6 相关载体或寡核苷酸处理。测定细胞的活力、迁移、侵袭和凋亡水平,测量上皮-间充质转化(EMT)相关蛋白的水平。验证 OIP5-AS1 和 miR-92a 之间以及 miR-92a 和 ITGA6 之间的相互作用。

结果

OIP5-AS1 和 ITGA6 在 OC 中上调,而 miR-92a 下调。抑制 OIP5-AS1 或下调 ITGA6 或上调 miR-92a 抑制 EMT、活力、迁移和侵袭,并促进 OC 细胞凋亡。OIP5-AS1 作为一种竞争性内源性 RNA 与 miR-92a 相互作用,调节 ITGA6。沉默 OIP5-AS1 诱导的这些作用可以通过抑制 miR-92a 逆转,而上调 miR-92a 诱导的作用可以通过恢复 ITGA6 减少。

结论

沉默 OIP5-AS1 通过抑制 ITGA6 促进 miR-92a 抑制 OC 细胞的增殖和转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb74/8848981/4f2f658a5a60/13048_2021_937_Fig1_HTML.jpg

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