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长链非编码RNA OIP5-AS1敲低靶向miR-183-5p/谷氨酰胺合成酶轴并抑制鼻咽癌细胞的增殖、迁移和转移

LncRNA OIP5-AS1 Knockdown Targets miR-183-5p/GLUL Axis and Inhibits Cell Proliferation, Migration and Metastasis in Nasopharyngeal Carcinoma.

作者信息

Li Shuo, Tang Mingxing, Zen Nan, Liang Junyi, Xing Xiao, Huang Danglin, Liu Fei, Zhang Xiaomeng

机构信息

Department of Otolaryngology, The 6th Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China.

Department of Otolaryngology, Huazhong University of Science and Technology Union Shenzhen Hospital, Shenzhen, China.

出版信息

Front Oncol. 2022 Jun 8;12:921929. doi: 10.3389/fonc.2022.921929. eCollection 2022.

Abstract

Nasopharyngeal carcinoma (NPC) is often associated with the infection of Epstein-Barr virus in nasopharynx and is mainly happened in South China and Southeast Asia. Recently, noncoding RNAs have been reported to regulate NPC carcinogenesis. LncRNA OIP5-AS1 participates in tumorigenesis and progression; however, the inherent mechanism of OIP5-AS1-mediated progression of NPC is unclear. In the current study, we aimed to explore the role of OIP5-AS1 in NPC progression. We measured the cell viability, apoptosis, migration, and invasion in NPC cells after OIP5-AS1 modulation. Moreover, we determined whether OIP5-AS1 exerts its oncogenic functions sponging miR-183-5p in NPC. Furthermore, we determined whether glutamate ammonia ligase (GLUL) was a downstream target of miR-183-5p. We found that OIP5-AS1 downregulation inhibited the viability, migration and invasion of NPC targeting miR-183-5p. We also identified that GLUL might be a potential downstream target of miR-183-5p in NPC cells. Mechanistically, OIP5-AS1 promotes cell motility regulating miR-183-5p and GLUL in NPC cells. We concluded that OIP5-AS1 performed its biological functions targeting miR-183-5p and GLUL in NPC cells.

摘要

鼻咽癌(NPC)常与鼻咽部的 Epstein-Barr 病毒感染相关,主要发生在中国南方和东南亚地区。最近,有报道称非编码 RNA 可调节鼻咽癌的发生发展。长链非编码 RNA OIP5-AS1 参与肿瘤的发生和进展;然而,OIP5-AS1 介导鼻咽癌进展的内在机制尚不清楚。在本研究中,我们旨在探讨 OIP5-AS1 在鼻咽癌进展中的作用。我们检测了 OIP5-AS1 调节后鼻咽癌细胞的活力、凋亡、迁移和侵袭情况。此外,我们确定 OIP5-AS1 是否通过在鼻咽癌中吸附 miR-183-5p 发挥其致癌功能。此外,我们确定谷氨酸氨连接酶(GLUL)是否为 miR-183-5p 的下游靶点。我们发现 OIP5-AS1 的下调通过靶向 miR-183-5p 抑制了鼻咽癌的活力、迁移和侵袭。我们还确定 GLUL 可能是鼻咽癌细胞中 miR-183-5p 的潜在下游靶点。机制上,OIP5-AS1 通过调节鼻咽癌细胞中的 miR-183-5p 和 GLUL 促进细胞运动。我们得出结论,OIP5-AS1 通过靶向鼻咽癌细胞中的 miR-183-5p 和 GLUL 发挥其生物学功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af90/9214031/89c9356b4e03/fonc-12-921929-g001.jpg

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