Objective: Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer. Long noncoding RNAs (lncRNAs) have been reported to be involved in the development of TNBC. However, the role and mechanism of LINC01096 in TNBC are largely unclear. This work aims to investigate the effect of LINC01096 on cell viability, apoptosis, migration, and invasion of TNBC cells, as well as explore the interaction between LINC01096 and microRNA (miR)-3130-3p.
Patients and methods: Sixty TNBC patients were recruited. T47-D and BT-549 cells were cultured for experiments in vitro. The expression levels of LINC01096 and miR-3130-3p were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability, apoptosis, migration, and invasion were determined by MTT, flow cytometry, and trans-well assays. The target association between LINC01096 and miR-3130-3p was confirmed by the luciferase reporter assay.
Results: The expression of LINC01096 was enhanced in TNBC tissues and cells. High expression of LINC01096 predicted poor outcomes of patients with TNBC. Silence of LINC01096 led to the suppression of cell viability, migration, and invasion, as well as the promotion of apoptosis in TNBC cells. MiR-3130-3p was targeted by LINC01096 and lowly expressed in TNBC. Overexpression of miR-3130-3p repressed cell viability, migration, and invasion, while it induced apoptosis. However, the knockdown of miR-3130-3p induced the opposite effect. This was weakened by inhibiting LINC01096.
Conclusions: Knockdown of LINC01096 inhibited cell viability, migration, and invasion; however, it promoted apoptosis in TNBC by up-regulating miR-3130-3p, indicating a novel target for the treatment of TNBC.