【Abstract】Objective To explore the effect and mechanism of longchain noncoding RNA TTNAS1 on breast cancer growth and metastasis. Methods QRTPCR was used to detect the expression level of TTNAS1 in 5 types of breast cancer cells. Transfection of breast cancer cells with shRNA inhibits the expression of TTN AS1. After transfection, CCK8 tested the proliferation ability of each group of cells. Western blot was used to detect the relative expression levels of apoptosisrelated proteins Bcl2, Bax, CleavedCaspase3, and Caspase3. The miRcode database predicts the binding sites of lncRNA TTNAS1 and miR1345p. The double luciferase reporter gene experiment verified the targeting relationship between lncRNA TTNAS1 and miR1345p. Transfection of shRNA in breast cancer cells inhibits the expression of TTNAS1 while transfection of miR1345p inhibitor inhibits the expression of miR1345p, and then detects changes in cell proliferation, apoptosis, migration ability and apoptosisrelated protein expression. Results TTN AS1 is highly expressed in 5 types of breast cancer cells. After inhibiting the expression of TTNAS1, the proliferation and migration ability of breast cancer cells was significantly downregulated, the level of cell apoptosis was significantly increased, the expression of Bcl2 was significantly downregulated, and the expression of Bax and CleavedCaspase3 were significantly upregulated (all P＜0 05). miR1345p is the target gene of lncRNA TTNAS1, inhibiting the expression of TTNAS1 while inhibiting the expression of miR1345p cell proliferation and migration were significantly higher than that of the TTNAS1 group alone, and the level of cell apoptosis was significantly lower In the TTNAS1 group alone, the expression of apoptosisrelated proteins also showed significant changes (all P＜005). Conclusion TTNAS1 regulates the proliferation, apoptosis, migration ability and expression of apoptosisrelated proteins of breast cancer cells through targeted inhibition of miR1345p.