Emerging evidence has illustrated that long noncoding RNA 01234 (LINC01234) has played a pivotal role in the development and progression of human cancer. The regulatory role and underlying mechanisms of LINC01234 in triple-negative breast cancer (TNBC) remains unknown. In this study, we analyzed the expression level of LINC01234 in several breast cancer cell lines. CCK-8, EdU, flow cytometry analysis, wound healing assay, and transwell assay were carried out to investigate the effect of LINC01234 on tumor proliferation, apoptosis, and migration. Bioinformatic analysis and luciferase reporter assays were performed to confirm the molecular binding. We found that LINC01234 was dramatically upregulated in breast cancer cell lines, especially in TNBC. The loss and gain-of functional experiments revealed that LINC01234 significantly promoted proliferation, migration, and suppressed cell apoptosis of MDA-MB-231 cells in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations demonstrated that LINC01234 might act as a competing endogenous RNA (ceRNA) for miR-429 to regulate the SYNJ1 expression. The effects of miR-429 and SYNJ1 in MDA-MB-231 cells were also analyzed. Our results revealed that the novel LINC01234/miR-429/SYNJ1 axis played a critical role in progression of TNBC cell line MDA-MB-231, and it may serve as a therapeutic target for TNBC.