Department of Reproductive Medicine, Luoyang Center Hospital Affiliated to Zhengzhou University, China.
Department of Reproductive Medicine, Luoyang Center Hospital Affiliated to Zhengzhou University, China.
Biomed Pharmacother. 2020 May;125:109839. doi: 10.1016/j.biopha.2020.109839. Epub 2020 Jan 29.
Increasing lncRNAs are found to be involved in the biological process of multiple cancer types. Herein, we aimed to reveal the role of LOXL1-AS1 in endometrial cancer (EC) progression.
Tumor and corresponding normal tissues were obtained from EC patients. Si-LOXL1-AS1 and miR-28-5p inhibitor were transfected to downregulate the expressions of LOXL1-AS1 and miR-28-5p, while miR-28-5p mimics were used to upregulate the miR-28-5p expression. CCK-8 and colony assays were applied to estimate the cell proliferation. Flow cytometry was performed to measure the cell apoptosis. Wound healing and transwell assays were conducted to assess the cell migration and invasion abilities. Informatics analysis was used to explore the relationship among LOXL1-AS1, miR-28-5p and RAP1B.
LOXL1-AS1 was found markedly up-regulated in EC tissues and cell lines. LOXL1-AS1 knockdown displayed evident suppression in cell proliferation, migration and invasion, as well as promotion in cell apoptosis. Moreover, the LOXL1-AS1 induced regulatory effects on EC cells were partially reversed by miR-28-5p inhibitor. Mechanistically, LOXL1-AS1 competitively bond to miR-28-5p, resulting in upregulation of RAP1B. Additionally, in vivo study confirmed the findings discovered in vitro.
In summary, LOXL1-AS1 exerted oncogenic roles in EC progression by sponging miR-28-5p and thereby upregulating RAP1B. This finding might provide potential targets for EC therapy.
越来越多的长链非编码 RNA 被发现参与多种癌症类型的生物学过程。在此,我们旨在揭示 LOXL1-AS1 在子宫内膜癌(EC)进展中的作用。
从 EC 患者中获得肿瘤和相应的正常组织。Si-LOXL1-AS1 和 miR-28-5p 抑制剂转染以下调 LOXL1-AS1 和 miR-28-5p 的表达,而 miR-28-5p 模拟物用于上调 miR-28-5p 的表达。CCK-8 和集落测定用于评估细胞增殖。流式细胞术用于测量细胞凋亡。伤口愈合和 Transwell 测定用于评估细胞迁移和侵袭能力。信息学分析用于探索 LOXL1-AS1、miR-28-5p 和 RAP1B 之间的关系。
发现 LOXL1-AS1 在 EC 组织和细胞系中明显上调。LOXL1-AS1 敲低显示细胞增殖、迁移和侵袭明显受到抑制,细胞凋亡明显增加。此外,miR-28-5p 抑制剂部分逆转了 LOXL1-AS1 对 EC 细胞的诱导调节作用。机制上,LOXL1-AS1 竞争性结合 miR-28-5p,导致 RAP1B 上调。此外,体内研究证实了体外发现的结果。
总之,LOXL1-AS1 通过海绵 miR-28-5p 发挥致癌作用,从而上调 RAP1B,在 EC 进展中发挥致癌作用。这一发现可能为 EC 治疗提供潜在的靶点。