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长链非编码 RNA FEZF1-AS1 通过调控 miR-130a-5p/SOX4 轴促进卵巢癌细胞的进展。

Long non-coding RNA FEZF1-AS1 induced progression of ovarian cancer via regulating miR-130a-5p/SOX4 axis.

机构信息

Department of Gynaecology and Obstetrics, China-Japan Union Hospital of Jilin University, Changchun, China.

出版信息

J Cell Mol Med. 2020 Apr;24(7):4275-4285. doi: 10.1111/jcmm.15088. Epub 2020 Mar 5.

DOI:10.1111/jcmm.15088
PMID:32135030
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7171310/
Abstract

Emerging studies have revealed the critical role of long non-coding RNAs (lncRNAs) in epithelial ovarian cancer (EOC) development and progression. Till now, the roles and potential mechanisms regarding FEZF1 antisense RNA 1 (FEZF1-AS1) within ovarian cancer (OC) remain unclear. The objective of this study was to uncover the biological function and the underlying mechanism of LncRNA FEZF1-AS1 in OC progression. FEZF1-AS1 expression levels were studied in cell lines and tissues of human ovarian cancer. In vitro studies were performed to evaluate the impact of FEZF1-AS1 knock-down on the proliferation, invasion, migration and apoptosis of OC cells. Interactions of FEZF1-AS1 and its target genes were identified by luciferase reporter assays. Our data showed overexpression of FEZF1-AS1 in OC cell lines and tissues. Cell migration, proliferation, invasion, wound healing and colony formation were suppressed by silencing of FEZF1-AS1. In contrast, cell apoptosis was promoted by FEZF1-AS1 knock-down in vitro. Furthermore, online bioinformatics analysis and tools suggested that FEZF1-AS1 directly bound to miR-130a-5p and suppressed its expression. Moreover, the inhibitory effects of miR-130a-5p on the OC cell growth were reversed by FEZF1-AS1 overexpression, which was associated with the increase in SOX4 expression. In conclusion, our results revealed that FEZF1-AS1 promoted the metastasis and proliferation of OC cells by targeting miR-130a-5p and its downstream SOX4 expression.

摘要

新兴研究揭示了长非编码 RNA（lncRNA）在卵巢上皮性癌（EOC）发展和进展中的关键作用。到目前为止，FEZF1 反义 RNA 1（FEZF1-AS1）在卵巢癌（OC）中的作用和潜在机制尚不清楚。本研究旨在揭示 LncRNA FEZF1-AS1 在 OC 进展中的生物学功能和潜在机制。研究了人卵巢癌细胞系和组织中的 FEZF1-AS1 表达水平。进行了体外研究，以评估 FEZF1-AS1 敲低对 OC 细胞增殖、侵袭、迁移和凋亡的影响。通过荧光素酶报告基因测定鉴定 FEZF1-AS1 及其靶基因之间的相互作用。我们的数据显示 FEZF1-AS1 在 OC 细胞系和组织中过表达。沉默 FEZF1-AS1 抑制细胞迁移、增殖、侵袭、伤口愈合和集落形成。相比之下，FEZF1-AS1 敲低在体外促进细胞凋亡。此外，在线生物信息学分析和工具表明，FEZF1-AS1 直接与 miR-130a-5p 结合并抑制其表达。此外，FEZF1-AS1 过表达逆转了 miR-130a-5p 对 OC 细胞生长的抑制作用，这与 SOX4 表达的增加有关。总之，我们的研究结果表明，FEZF1-AS1 通过靶向 miR-130a-5p 及其下游 SOX4 表达促进 OC 细胞的转移和增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/10dae7389aa1/JCMM-24-4275-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/2478ff2ca4f8/JCMM-24-4275-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/2cf2759e343b/JCMM-24-4275-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/8a19a945828c/JCMM-24-4275-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/d1c1828de6b7/JCMM-24-4275-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/f43f0dd42a6d/JCMM-24-4275-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/62cdd97e20f0/JCMM-24-4275-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/10dae7389aa1/JCMM-24-4275-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/2478ff2ca4f8/JCMM-24-4275-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/2cf2759e343b/JCMM-24-4275-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/8a19a945828c/JCMM-24-4275-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/d1c1828de6b7/JCMM-24-4275-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/f43f0dd42a6d/JCMM-24-4275-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/62cdd97e20f0/JCMM-24-4275-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a2c/7171310/10dae7389aa1/JCMM-24-4275-g007.jpg

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