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Research Paper|Volume 12, Issue 14|pp 14775—14790

The circular RNA circEIF3M promotes breast cancer progression by promoting cyclin D1 expression

Xiujuan Li1, Zhaojun Ren2, Yufeng Yao1, Jun Bao3, Qiao Yu1
  • 1Department of General Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China
  • 2Department of Pathology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China
  • 3Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China
* Equal contribution
Received: January 1, 2020Accepted: May 20, 2020Published: July 11, 2020
https://doi.org/10.18632/aging.103539

Copyright: © 2020 Li 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

We investigated the function of circular RNA circEIF3M (hsa_circ_0003119) in triple-negative breast cancer. The expression profiles of circRNAs in 3 specimens of triple-negative breast cancer tissues with adjacent nontumor tissues were analyzed by RNA-sequencing. We verified the oncogenic role of circEIF3M in triple-negative breast cancer through a series of biological function experiments. It was found that circEIF3M was markedly upregulated in triple-negative breast cancer as compared to adjacent nontumor tissue, and that circEIF3M promoted triple-negative breast cancer cell proliferation, migration, and invasion. Mechanistic analysis indicated that circEIF3M may act as a competing endogenous RNA for miR-33a that relieves the inhibitory effect of miR-33a on its target cyclin D1. These findings showed that circEIF3M promotes triple-negative breast cancer progression via the circEIF3M/ miR-33a/ cyclin D1 axis.