Objective To investigate the effects and mechanisms of LncRNA XIST on proliferation, migration, invasion and apoptosis of breast cancer cells.

Methods Normal mammary epithelial cells MCF-10A and breast cancer cell lines MCF-7, T47D and Bcap-37 cells were selected and transfected into MCF-7 and T47D cells with different substances. They were set as blank group (no transfection), si-XIST group (transfection si-XIST), si-NC group (transfection si-NC), microRNA-20a-5p group (transfection miR-20a-5p mimics) and miR-NC group (transfection miR-NC). CCK-8 was used to detect cell proliferation; Transwell was used to detect cell invasion ability; cell migration ability was detected by scratch test; apoptosis was detected by TUNEL staining. Luciferase reporter gene assay was used to verify the targeting relationships between LncRNA XIST and miR-20a-5p as well as between miR-20a-5p and high mobility group protein A2 (HMGA2). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of LncRNA XIST and miR-20a-5p. The expression level of HMGA2 was detected by Western blot.

Results Compared with MCF-10A cells, LncRNA XIST expression levels in MCF-7, T47D and Bcap-37 cells were significantly increased, while miR-20a-5p expression level was significantly decreased (P < 0.05). Down-regulating LncRNA XIST or up-regulating miR-20a-5p inhibited proliferation, invasion and migration of breast cancer cells, and promoted cell apoptosis (P < 0.05). LncRNA XIST negatively regulated miR-20a-5p, and miR-20a-5p negatively regulated HMGA2.

Conclusion Down-regulated LncRNA XIST inhibits proliferation, migration andinvasion of breast cancer cells and promotes cell apoptosis through miR-20a-5p/HMGA2 axis.