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Research Paper|Volume 12, Issue 11|pp 10983—11003

The circRNA circIFI30 promotes progression of triple-negative breast cancer and correlates with prognosis

Lei Xing1, Rui Yang2, Xiaosong Wang2, Xiaying Zheng2, Xin Yang3, Luyu Zhang4, Rong Jiang5, Guosheng Ren1, Junxia Chen2
  • 1Department of Endocrine and Breast Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China
  • 2Department of Cell Biology and Genetics, Chongqing Medical University, Chongqing, China
  • 3Department of Thoracic Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China
  • 4Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China
  • 5Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China
Received: January 18, 2020Accepted: March 31, 2020Published: June 4, 2020
https://doi.org/10.18632/aging.103311

Copyright © 2020 Xing 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

Growing evidence suggests that circRNAs exert a critical role in tumorigenesis and cancer progression. To date, the molecular mechanisms underlying circRNAs in triple-negative breast cancer (TNBC) are still poorly known. Here, circRNA expression profile was investigated by RNA sequencing in TNBC tissues and matched para-carcinoma tissues. We found that circIFI30 was significantly up-regulated in TNBC tissues and cells using quantitative real-time PCR and in situ hybridization. High circIFI30 expression was positively correlated with clinical TNM stage, pathological grade and poor prognosis of TNBC patients. Functionally, a series of in vivo and in vitro experiments showed that knockdown of circIFI30 could markedly inhibit TNBC cell proliferation, migration, invasion and cell cycle progression, induce apoptosis as well as suppress tumorigenesis and metastasis. Up-regulation of circIFI30 exerted an opposite effect. Mechanistically, we demonstrated that circIFI30 might act as a competing endogenous RNA (ceRNA) of miR-520b-3p to abolish the suppressive effect on target gene CD44 by fluorescent in situ hybridization (FISH), dual luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assays. Therefore, our work uncovers the mechanism by which circIFI30 could promote TNBC progression through circIFI30/miR-520b-3p/CD44 axis and circIFI30 could be a novel diagnostic/prognostic marker and therapeutic target for TNBC patients.