Open Access

ARTICLE

Long noncoding RNA CCDC183-AS1 depletion represses breast cancer cell proliferation, colony formation, and motility by sponging microRNA-3918

TAO LIU¹, LIMIN ZHOU¹, LIANBO ZHANG², XIN GUAN³, YI DONG^1,*

1 Department of Second Breast Surgery, Jilin Cancer Hospital, Changchun, 130012, China
2 Medical Insurance Guarantee Office, Jilin Cancer Hospital, Changchun, 130012, China
3 Department of Breast Surgery, The First Hospital of Jilin University, Changchun, 130061, China

* Corresponding Author: Yi Dong,

Oncology Research 2021, 29(3), 189-200. https://doi.org/10.32604/or.2022.03573

Received 28 April 2022; Accepted 27 June 2022; Issue published 01 August 2022

Abstract

Many studies have illustrated the significance of long noncoding RNAs in oncogenesis and promotion of breast cancer (BC). However, the biological roles of CCDC183 antisense RNA 1 (CCDC183-AS1) in BC have rarely been characterized. Thus, we explored whether CCDC183-AS1 is involved in the malignancy of BC and elucidated the possible underlying mechanisms. Our data confirmed elevated CCDC183-AS1 expression in BC, which was associated with poor clinical outcomes. Functionally, knocking down CCDC183-AS1 hampered cell proliferation, colony formation, migration, and invasion in BC. Additionally, the absence of CCDC183-AS1 restrained tumor growth in vivo. Mechanistically, CCDC183-AS1 executed as a competitive endogenous RNA in BC cells by decoying microRNA-3918 (miR-3918) and consequently overexpressing fibroblast growth factor receptor 1 (FGFR1). Furthermore, functional rescue experiments confirmed that inactivation of the miR-3918/FGFR1 regulatory axis by inhibiting miR-3918 or increasing FGFR1 expression could abrogate the CCDC183-AS1 ablation-mediated repressive effects in BC cells. In summary, CCDC183-AS1 deteriorates the malignancy of BC cells by controlling miR-3918/FGFR1 regulatory axis. We believe that our study can deepen our understanding of BC etiology and contribute to an improvement in treatment choices.

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