Abstract
BACKGROUND The oncogenic roles of lncRNA THOR have been revealed in several tumors, however, its functions in breast cancer are still unclear. MATERIAL AND METHODS Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect THOR expression in clinical samples and the expression of stemness regulatory factors. ALDH1 assay and sphere-formation analysis were constructed to examine the stemness of cells. Cell viability assay was constructed to determine the cell proliferation capacity. In vitro RNA-RNA interaction and messenger RNA (mRNA) stability assays were performed to explore the mechanisms. RESULTS THOR was overexpressed in triple-negative breast cancer (TNBC) compared to that in luminal A- and B-type breast cancer. THOR silencing reduced TNBC cell stemness, which was evident by the decreased sphere-formation ability, stemness marker expression and ALDH1 activity. Mechanistically, THOR directly bound to ß-catenin mRNA, enhanced ß-catenin mRNA stability and thus increased its expression. Furthermore, overexpression of ß-catenin partially diminished THOR silencing-mediated inhibition on TNBC cell stemness. CONCLUSIONS This work proposes that THOR facilitates TNBC cell stemness through activating ß-catenin signaling.