Tumor protein D52 promotes breast cancer proliferation and migration via the long non-coding RNA NEAT1/microRNA-218-5p axis.

Abstract

BackgroundBreast cancer is an aggressive disease with high morbidity and mortality rates among women globally. Tumor protein D52 (TPD52) is an oncogene in breast cancer; however, its physiological function remains elusive. This study set out to obtain a deeper understanding of the functions of TPD52 in the pathophysiology of breast cancer by exploring its effects on breast cancer cell proliferation and migration.MethodsBioinformatics analysis was performed to predict the bonding of TPD52 and nuclear paraspeckle assembly transcript 1 (NEAT1) with miR-218-5p. The bonding of TPD52 and NEAT1 with miR-218-5p were verified by luciferase reporter assays. The mRNA expression of TPD52, miR-218-5p or NEAT1 were tested by Rt-qPCR and the protein expression of TPD52 was tested by western blot. Colony formation and EdU assays were carried out to evaluate cell proliferation. Wound healing and Transwell assays were used to evaluate migration.ResultsIn this study, TPD52 was upregulated in breast cancer cells, and silencing of TPD52 repressed the proliferation and migration of breast cancer cells in vitro and in vivo. Further, microRNA (miR)-218-5p reduced the expression level of TPD52, while overexpression of TPD52 attenuated the effects of miR-218-5p mimics on breast cancer cell proliferation and migration. Also, NEAT1 acted as a competitive endogenous sponge of miR-218-5p to downregulate free miR-218-5p levels. It was further observed that TPD52 overexpression recovered the inhibition of breast cancer cell growth and migration caused by NEAT1 downregulation. These results confirmed the functions of NEAT1 in breast cancer and supported the mechanism of the NEAT1/miR-218-5p/TPD52 axis.ConclusionsOur findings highlight the important role of the NEAT1/miR-218-5p/TPD52 axis in breast cancer cell proliferation and migration. This axis may be a potential therapeutic target for breast cancer.