1 贵州省肿瘤医院乳腺外科，贵阳 550003
2 贵州医科大学附属医院乳腺外科，贵阳 550004
Effect of silencing lncRNA THAP9-AS1 on the proliferation, apoptosis, migration and invasion of breast cancer cells
CorrespondingAuthor: YANG Haisong Email: Yanghaisong609@sina.com
Objective: To explore the effect of silencing lncRNA THAP9-AS1 on the proliferation, apoptosis, migration and invasion of breast cancer cells. Methods: The cancer tissues and adjacent tissues were collected from 25 breast cancer patients at Guizhou Cancer Hospital from June 2017 to June 2020. The expression levels of lncRNA THAP9-AS1 and miR-505-3p were detected by real-time quantitative polymerase chain reaction (RT-qPCR). MDA-MB-231 cells were randomly divided into the si-THAP9-AS1 group, the si-NC group, the miR-505-3p group, the miR-NC group, the si-THAP9-AS1 + anti-miR-NC group, and the si-THAP9-AS1 + miR-505-3p inhibitor group. Cell activity was detected by methyl thiazolyl tetrazolium (MTT) method; cell colony formation was detected by plate cloning assay; cell apoptosis was detected by flow cytometry assay; cell migration and invasion were detected by scratching assay and Transwell assay; dual luciferase reporting assay was used to detect the targeting relationship between lncRNA THAP9-AS1 and miR-505-3p. Results: The expression level of lncRNA THAP9-AS1 was increased in breast cancer tissues compared with adjacent tissues, while the expression level of miR-505-3p was decreased (P<0.05). Silencing lncRNA THAP9-AS1 or miR-505-3p overexpression could inhibit cell viability and migration, decrease the number of colonies and invaded cells, increase the rate of apoptosis and the protein level of E-cadherin, and reduce the protein level of N-cadherin (P<0.05). Moreover, lncRNA THAP9-AS1 targeted miR-505-3p, and inhibition of miR-505-3p reversed the effects of lncRNA THAP9-AS1 silence on the proliferation, migration and invasion of MDA-MB-231 cells. Conclusion: Silencing lncRNA THAP9-AS1 can inhibit the proliferation, migration and invasion and promote apoptosis of breast cancer cells by up-regulating miR-505-3p.