Abnormal expression of long non-coding RNA FGD5-AS1 affects the development of ovarian cancer through regulating miR-107/RBBP6 axis.

IF 1.6 4区医学 Q4 PHYSIOLOGY Chinese Journal of Physiology Pub Date : 2023-05-01 DOI:10.4103/cjop.CJOP-D-22-00084

Wen Zhang, Jianguo Shi, Guoyan Liu

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Abstract

Long non-coding RNAs (lncRNAs) are important players in cancer development. LncRNA FGD5-AS1 has been reported as a potential oncogene in ovarian cancer (OC). The present paper focused on the action mechanism of FGD5-AS1 in OC. Clinical OC samples were collected for expression analyses of FGD5-AS1, RBBP6, and miR-107. The expression of FGD5-AS1, RBBP6, and miR-107 in OC cells was altered by transfection. OC cell proliferation was assessed by MTT and colony formation assays, and angiogenesis of human umbilical vein endothelial cells (HUVECs) cultured with OC cell supernatants by matrigel angiogenesis assay. The interactions among FGD5-AS1, miR-107, and RBBP6 were detected by luciferase reporter assay. FGD5-AS1 and RBBP6 were strongly expressed and miR-107 was poorly expressed in clinical OC samples and OC cell lines. FGD5-AS1 or RBBP6 overexpression in Hey and SKOV3 cells could potentiate OC cell proliferation and HUVEC angiogenesis, while FGD5-AS1 or RBBP6 knockdown in OC cells inhibited the above cellular processes. FGD5-AS1 targeted miR-107 to positively regulate RBBP6 expression. Additionally, miR-107 overexpression or RBBP6 knockdown in SKOV3 cells partially reversed the FGD5-AS1-dependent stimulation of OC cell proliferation and HUVEC angiogenesis. FGD5-AS1 may act as a promoter of OC via miR-107/RBBP6 axis.

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长链非编码RNA FGD5-AS1的异常表达通过调控miR-107/RBBP6轴影响卵巢癌的发生发展。

长链非编码rna (lncRNAs)在癌症发展中起着重要作用。LncRNA FGD5-AS1已被报道为卵巢癌(OC)的潜在致癌基因。本文主要探讨FGD5-AS1在OC中的作用机制。收集临床OC样本进行FGD5-AS1、RBBP6和miR-107的表达分析。转染后，OC细胞中FGD5-AS1、RBBP6和miR-107的表达发生改变。MTT法和集落形成法检测脐静脉内皮细胞的增殖，基质血管生成法检测脐静脉内皮细胞(HUVECs)的血管生成。通过荧光素酶报告基因法检测FGD5-AS1、miR-107和RBBP6之间的相互作用。FGD5-AS1和RBBP6在临床OC样品和OC细胞系中表达强烈，miR-107表达低。FGD5-AS1或RBBP6在Hey和SKOV3细胞中过表达可促进OC细胞增殖和HUVEC血管生成，而FGD5-AS1或RBBP6在OC细胞中下调可抑制上述细胞过程。FGD5-AS1靶向miR-107正向调节RBBP6的表达。此外，SKOV3细胞中miR-107过表达或RBBP6敲低部分逆转了fgd5 - as1依赖性OC细胞增殖和HUVEC血管生成的刺激。FGD5-AS1可能通过miR-107/RBBP6轴作为OC的启动子。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Chinese Journal of Physiology 医学-生理学

CiteScore

2.30

自引率

5.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Chinese Journal of Physiology is a multidisciplinary open access journal. Chinese Journal of Physiology (CJP) publishes high quality original research papers in physiology and pathophysiology by authors all over the world. CJP welcomes submitted research papers in all aspects of physiology science in the molecular, cellular, tissue and systemic levels. Multidisciplinary sciences with a focus to understand the role of physiology in health and disease are also encouraged. Chinese Journal of Physiology accepts fourfold article types: Original Article, Review Article (Mini-Review included), Short Communication, and Editorial. There is no cost for readers to access the full-text contents of publications.