MIR210HG 通过调控 miR-503-5p/TRAF4 轴促进宫颈癌的细胞增殖和侵袭。

MIR210HG promotes cell proliferation and invasion by regulating miR-503-5p/TRAF4 axis in cervical cancer.

机构信息

Department of Gynecologic and Obstetrics, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang 471000, Henan, China.

Department of Gynecologic and Obstetrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.

出版信息

Aging (Albany NY). 2020 Feb 21;12(4):3205-3217. doi: 10.18632/aging.102799.

Long non-coding RNAs (lncRNAs) play important roles in the progression of cervical cancer (CC). However, the roles and underlying molecular mechanisms of lncRNAs in CC remain unclear. In the current study, we discovered a new lncRNA MIR210HG which was upregulated in CC tissues through microarray. The upregulation of MIR210HG was associated with advanced FIGO stage, metastasis, and poor prognosis in CC patients. Function assays showed that MIR210HG inhibition significantly suppressed the proliferation, invasion, and epithelial-mesenchymal transition (EMT) processes in CC and reduced tumor growth in vivo. Mechanistically, we identified that MIR210HG might serve as a competing endogenous RNA (ceRNA) of miR-503-5p to relieve the repressive effect of miR-503-5p on TRAF4 expression in CC cells. In conclusion, we demonstrated that MIR210HG promoted CC progression through regulating the MIR210HG/miR-503-5p/TRAF4 axis, indicating that MIR210HG might act as a novel insight into CC treatment.

长链非编码 RNA（lncRNA）在宫颈癌（CC）的进展中发挥重要作用。然而，lncRNA 在 CC 中的作用及其潜在的分子机制尚不清楚。在本研究中，我们通过微阵列发现了一种新的 lncRNA MIR210HG，其在 CC 组织中上调。MIR210HG 的上调与 CC 患者FIGO 晚期、转移和预后不良相关。功能分析表明，MIR210HG 的抑制显著抑制了 CC 中的增殖、侵袭和上皮-间充质转化（EMT）过程，并减少了体内肿瘤的生长。机制上，我们确定 MIR210HG 可能作为 miR-503-5p 的竞争性内源性 RNA（ceRNA），以减轻 miR-503-5p 对 CC 细胞中 TRAF4 表达的抑制作用。总之，我们证明 MIR210HG 通过调节 MIR210HG/miR-503-5p/TRAF4 轴促进 CC 进展，表明 MIR210HG 可能成为 CC 治疗的新靶点。