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.