Copyright (c) 2023 Mei Peng, Hao Yuan
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.LncRNA PSMA3-AS1 activates the progression of triple-negative breast cancer cells by blocking miR-186-5p-mediated PSME3 inhibition
Corresponding Author(s) : Hao Yuan
Cellular and Molecular Biology,
Vol. 69 No. 14: Cancer molecular biology: Diagnosis and treatment
Abstract
Triple-negative breast cancer (TNBC) is an aggressive malignant tumor with a high death rate in the whole world. This cancer mainly occurs in young women group possessed with poor prognoses. Long noncoding RNAs (lncRNAs) are known for regulating human diseases and cancers. Even though growing researches have illuminated that lncRNAs have a close relation with TNBC progression, the function of lncRNAPSMA3 antisense RNA 1 (PSMA3-AS1) in TNBC has not been discussed and exposed yet. In the present research, the expression pattern and functional role of PSMA3-AS1 were analyzed and unveiled with the help of RT-qPCR and functional assays. The findings demonstrated that PSMA3-AS1 was notably upregulated in TNBC cells. Silencing of PSMA3-AS1 had suppressing effects on TNBC cell growth and migration. Mechanistically, PSMA3-AS1 induced upregulation of proteasome activator subunit 3 (PSME3) by functioning as a miR-186-5p sponge. Furthermore, rescue assays certified that overexpression of PSME3 or inhibition of miR-186-5p could abrogate the inhibiting role of silenced PSMA3-AS1 on TNBC cell functions. To summarize, PSMA3-AS1 abolishes miR-186-5p-mediated suppression on PSME3 to accelerate TNBC progression.
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