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Research Paper|Volume 11, Issue 14|pp 4858—4875

CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Chunyong Han1, Xuebiao Li2, Qian Fan3, Guangshu Liu4, Jian Yin1
  • 1Department of Breast Reconstruction, The Sino-Russian Joint Research Center for Oncoplastic Breast Surgery, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Treatment of Tianjin; Tianjin Clinical Research Center for Cancer; Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin 300060, China
  • 2Department of Cardiovascular Surgery, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310009, China
  • 3Department of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Treatment of Tianjin, Tianjin 300060, China
  • 4Department of Oncology, People's Hospital of Langfang City, Langfang 65000, China
Received: March 26, 2019Accepted: July 1, 2019Published: July 16, 2019
https://doi.org/10.18632/aging.102080

Copyright © 2019 Han et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Long non-coding RNAs (lncRNAs) regulate cancer development and progression. Here, we investigated the role of the lncRNA CCAT1 in triple-negative breast cancer (TNBC). CCAT1 expression was higher in TNBC cells than normal breast epithelial cells. Additionally, CCAT1 expression was higher in TNBC patient tumor tissue than adjacent normal breast tissue. Silencing CCAT1 inhibited TNBC cell proliferation, migration, and invasion in vitro, and tumor growth and progression in vivo. Bioinformatics analysis revealed that microRNA-218 (miR-218) is a potential target of CCAT1. Silencing CCAT1 resulted in an increase in miR-218 expression and inhibited TNBC cell proliferation, migration, and invasion. Silencing miR-218 reversed the effects of CCAT1 knockdown on cell proliferation, migration, and invasion, suggesting that CCAT1 promotes TNBC progression by downregulating miR-218 expression. We identified the zinc finger protein ZFX as a putative downstream target of miR-218 through bioinformatics analysis. ZFX expression was higher in TNBC than normal breast cell lines and higher in TNBC tumor tissue than adjacent normal breast tissue. Overexpression of ZFX reversed the tumor-suppressive effects of miR-218 on TNBC cell proliferation, migration, and invasion. Our data indicate that CCAT1 promotes TNBC progression by targeting the miR-218/ZFX axis.