@Article{or.2022.03573,
AUTHOR = {TAO LIU, LIMIN ZHOU, LIANBO ZHANG, XIN GUAN, YI DONG},
TITLE = {Long noncoding RNA CCDC183-AS1 depletion represses breast cancer cell proliferation, colony formation, and motility by sponging microRNA-3918},
JOURNAL = {Oncology Research},
VOLUME = {29},
YEAR = {2021},
NUMBER = {3},
PAGES = {189--200},
URL = {http://www.techscience.com/or/v29n3/49187},
ISSN = {1555-3906},
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 <i>in vivo</i>.
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.},
DOI = {10.32604/or.2022.03573}
}