LINC02159 modulated the glycolysis and proliferation of TNBC cell via targeting miR-1285-3p/G6PI axis.

As a leading cause of cancer-related fatalities among women, triple negative breast cancer (TNBC) still remains a clinical challenge. Increasing evidence points to long non-coding RNAs (lncRNAs) as significant regulators in its progression. The aim of this study is to investigate the function and working mechanism of LINC02159 in TNBC. The expression of LINC02159 in TNBC tissues and cells was detected by RT-qPCR analysis. Regulation of LINC02159 on TNBC is determined by the in vitro proliferation and migration assay. Binding of LINC02159 with the targets was tested by the luciferase reporter assay. The function of LINC02159 in the glycolysis of TNBC cells was evaluated via detecting the glucose uptake and lactate production. Our study identified that LINC02159 is overexpressed in TNBC tissues and correlates with decreased overall survival in patients. Functionally, silencing LINC02159 reduced TNBC cell proliferation and migration in vitro and suppressed the tumor growth in vivo. By acting as a competing endogenous RNA (ceRNA), LINC02159 directly engaged with miR-1285-3p to increase the expression of Glucose-6-phosphate isomerase (G6PI). In line with G6PI's role in glycolysis, reducing LINC02159 expression decreased glucose uptake and lactate production in TNBC cells. Restoring G6PI greatly reversed the impact of LINC02159 silencing on the proliferation and glycolysis of TNBC cells. These results demonstrated that LINC02159 drives the aerobic glycolysis and TNBC progression via modulating the miR-1285-3p/G6PI axis, and it might act as a potential target for TNBC anti-tumor therapy.