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lncRNA OIP5-AS1 Suppresses Cell Proliferation and Invasion of Endometrial Cancer by Regulating PTEN/AKT via Sponging miR-200c-3p
Journal of Immunology Research ( IF 4.1 ) Pub Date : 2021-07-29 , DOI: 10.1155/2021/4861749
Yun Liu 1 , Xiaohui Cai 1 , Yixuan Cai 1 , Yue Chang 1
Affiliation  

Background. Endometrial carcinoma (EC) is one of the major gynecologic malignancy cancers affecting females with dismal prognosis and high mortality around the world. Numerous studies have proven that an aberrant level of long noncoding RNAs is present in many endometrial cancer patients, while the underlying molecular mechanism remains unclear. Method. The expression levels of lncRNA OIP5-AS1, miR200c-3p, and PTEN were measured by a quantitative real-time polymerase chain reaction in endometrial cancer tissue and endometrial cancer cells. CCK8 assay, wound-healing assay, and cell colony formation were applied to evaluate cell proliferation, cell migration, and cell colony formation ability. Cell cycle and cell apoptosis were detected by flow cytometry. The interactions between OIP5-AS1, miR200c-3p, and PTEN were explored by luciferase activity. Results. In the present study, we demonstrated that long noncoding RNA OIP5-AS1 was significantly reduced in EC tissue compared with normal tissue. The lower expression level of OIP5-AS1 was also confirmed in four kinds of EC cell lines compared with the normal endometrial cell line. Gain- and loss-of-function of experiments indicated that upregulation of OIP5-AS1 could inhibit the proliferation, migration, and invasion of EC cells in vitro. Meanwhile, overexpression of OIP5-AS1 could also suppress the growth of tumor in the xenograft model. Moreover, further study revealed that miR-200c-3p could bind to OIP5-AS1, and the loss function of miR-200c-3p could reverse the elevated OIP5-AS1’s inhibitory effect on the progression of EC. Furthermore, we found that downregulation of miR-200c-3p was inversely correlated with PTEN expression in EC cells. Reduced OIP5-AS1 could lead to the accumulation of miR-200c-3p, which could induce the upregulation of PTEN indirectly. Conclusion. Our study demonstrated a novel molecular mechanism that lncRNA OIP5-AS1 could modulate the progression of EC by combining competitively with miR-200c-3p to control the PTEN/AKT pathway in EC cells, which might supply important information for developing novel therapeutic strategies for EC patients.

中文翻译:

lncRNA OIP5-AS1 通过海绵化 miR-200c-3p 调节 PTEN/AKT 抑制细胞增殖和子宫内膜癌的侵袭

背景。子宫内膜癌(EC)是影响女性的主要妇科恶性肿瘤之一,在世界范围内预后不佳,死亡率很高。大量研究证明,许多子宫内膜癌患者中存在异常水平的长链非编码 RNA,而其潜在的分子机制仍不清楚。方法. 通过定量实时聚合酶链反应测量子宫内膜癌组织和子宫内膜癌细胞中 lncRNA OIP5-AS1、miR200c-3p 和 PTEN 的表达水平。应用CCK8测定、伤口愈合测定和细胞集落形成来评估细胞增殖、细胞迁移和细胞集落形成能力。流式细胞仪检测细胞周期和细胞凋亡。通过荧光素酶活性探索 OIP5-AS1、miR200c-3p 和 PTEN 之间的相互作用。结果. 在本研究中,我们证明与正常组织相比,EC 组织中的长链非编码 RNA OIP5-AS1 显着减少。与正常子宫内膜细胞系相比,OIP5-AS1 在四种 EC 细胞系中的表达水平也较低。实验的增益和功能丧失表明OIP5-AS1的上调可以抑制体外EC细胞的增殖、迁移和侵袭. 同时,OIP5-AS1的过表达也可以抑制异种移植模型中肿瘤的生长。此外,进一步的研究表明,miR-200c-3p可以与OIP5-AS1结合,miR-200c-3p的丧失功能可以逆转升高的OIP5-AS1对EC进展的抑制作用。此外,我们发现 miR-200c-3p 的下调与 EC 细胞中 PTEN 的表达呈负相关。减少的 OIP5-AS1 可能导致 miR-200c-3p 的积累,这可能间接诱导 PTEN 的上调。结论. 我们的研究证明了一种新的分子机制,即 lncRNA OIP5-AS1 可以通过与 miR-200c-3p 竞争性结合来调节 EC 的进展,从而控制 EC 细胞中的 PTEN/AKT 通路,这可能为开发新的 EC 治疗策略提供重要信息。耐心。
更新日期:2021-07-29
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