Novel lncRNA PSMG3‑AS1 functions as a miR‑143‑3p sponge to increase the proliferation and migration of breast cancer cells.

Abstract

Long non-coding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3-antisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3-AS1 and microRNA (miR)-143-3p were determined using reverse-transcription quantitative PCR. The protein expression levels of collagen type 1 alpha 1 (COL1A1) and proliferating cell nuclear antigen (PCNA) were obtained using western blot analysis. Bioinformatics analysis was used to identify the relationship between PSMG3-AS1, miR-143-3p and COL1A1. Colony forming and Cell Counting Kit-8 assays were used to detect cell proliferation. Transwell and wound-healing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3-AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR-143-3p was decreased. Knockdown of PSMG3-AS1 increased the level of miR-143-3p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3-AS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miR-143-3p mimic transfection reduced proliferation and migration in MDA-MB-231 and MCF-7 cell lines. Furthermore, miR-143-3p inhibition significantly increased the proliferation and migration of breast cancer cells compared with the negative control group. The mRNA and protein expression levels of PCNA were reduced in the MCF-7 cell line when transfected with miR-143-3p mimics and si-PSMG3-AS1. However, PCNA expression was increased in cells transfected with a miR-143-3p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3-AS1, which serves as a sponge for miR-143-3p in the pathogenesis of breast cancer. PSMG3-AS1 may be used as a potential therapeutic target gene in breast cancer treatment.