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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 DONG1,*

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, email

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

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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Cite This Article

LIU, T., ZHOU, L., ZHANG, L., GUAN, X., DONG, Y. (2021). Long noncoding RNA CCDC183-AS1 depletion represses breast cancer cell proliferation, colony formation, and motility by sponging microRNA-3918. Oncology Research, 29(3), 189–200.



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