Research Paper Volume 12, Issue 4 pp 3205—3217

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

Ai-Hong Wang 1, 2, , Can-Hui Jin 3, , Guan-Yi Cui 4, , Hong-Yu Li 2, , Yin Wang 1, , Juan-Juan Yu 1, , Rui-Fang Wang 1, , Xiao-Yu Tian 1, ,

  • 1 Department of Gynecologic and Obstetrics, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang 471000, Henan, China
  • 2 Department of Gynecologic and Obstetrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China
  • 3 Department of Gastrointestinal Tumor Surgery, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang 471000, Henan,China
  • 4 University Hospital, Henan University of Science and Technology, Luoyang 471000, Henan, China

received: November 19, 2019 ; accepted: January 12, 2020 ; published: February 21, 2020 ;

https://doi.org/10.18632/aging.102799
How to Cite

Copyright © 2020 Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.

Abbreviations

CCK-8: Cell Counting Kit-8; qPCR: Quantitative reverse transcription polymerase chain reaction; ceRNA: Competing endogenous RNA; EdU: Ethynyl-2-deoxyuridine; lncRNA: Long non-coding RNA.