[No authors listed]
Long nonâcoding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3âantisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3âAS1 and microRNA (miR)â143â3p were determined using reverseâtranscription 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 PSMG3âAS1, miRâ143â3p and COL1A1. Colony forming and Cell Counting Kitâ8 assays were used to detect cell proliferation. Transwell and woundâhealing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3âAS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miRâ143â3p was decreased. Knockdown of PSMG3âAS1 increased the level of miRâ143â3p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3âAS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miRâ143â3p mimic transfection reduced proliferation and migration in MDAâMBâ231 and MCFâ7 cell lines. Furthermore, miRâ143â3p 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 MCFâ7 cell line when transfected with miRâ143â3p mimics and siâPSMG3âAS1. However, PCNA expression was increased in cells transfected with a miRâ143â3p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3âAS1, which serves as a sponge for miRâ143â3p in the pathogenesis of breast cancer. PSMG3âAS1 may be used as a potential therapeutic target gene in breast cancer treatment.
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