GUSBP11 Inhibited The Progression of Triple Negative Breast Cancer via Targeting The miR-579-3p/SPNS2 Axis

OBJECTIVE: Growing evidences have exposed the important roles of long noncoding RNAs (lncRNAs) in the triple negative breast cancer (TNBC) inhibition. The function of glucuronidase beta pseudogene 11 (GUSBP11) in the TNBC occurrence remains obscure. To detect the function of GUSBP11 in TNBC progression and explore its downstream molecular mechanism. MATERIALS AND METHODS: In this experimental study, using quantitative reverse transcription real-time polymerase chain reaction (RT-qPCR), we measured the GUSBP11 expression in the TNBC cell lines. Gain-of-function assays, including colony formation, flow cytometry, and western blot were used to identify the probable effects of GUSBP11 overexpression on the malignant behaviors of TNBC cell lines. Moreover, mechanism assays, including RNA immunoprecipitation (RIP), RNA pull down and luciferase reporter assays were taken to measure the possible mechanism of GUSBP11 in the TNBC cell lines. RESULTS: GUSBP11 expressed at a low RNA level in the TNBC cell lines. Overexpression of GUSBP11 RNA expression inhibited the proliferation, migration, epithelial-to-mesenchymal transition (EMT) and stemness while elevated the apoptosis of the TNBC cell lines. GUSBP11 positively regulated the expression of sphingolipid transporter 2 (SPNS2) via acting as a competing endogenous RNA (ceRNA) of miR-579-3p, thereby suppressing the development of TNBC cell lines. CONCLUSION: GUSBP11 impedes TNBC progression via modulating the miR-579-3p/SPNS2 axis.