RESUMO
Long noncoding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3antisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3AS1 and microRNA (miR)1433p were determined using reversetranscription 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 PSMG3AS1, miR1433p and COL1A1. Colony forming and Cell Counting Kit8 assays were used to detect cell proliferation. Transwell and woundhealing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR1433p was decreased. Knockdown of PSMG3AS1 increased the level of miR1433p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3AS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miR1433p mimic transfection reduced proliferation and migration in MDAMB231 and MCF7 cell lines. Furthermore, miR1433p 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 MCF7 cell line when transfected with miR1433p mimics and siPSMG3AS1. However, PCNA expression was increased in cells transfected with a miR1433p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3AS1, which serves as a sponge for miR1433p in the pathogenesis of breast cancer. PSMG3AS1 may be used as a potential therapeutic target gene in breast cancer treatment.