Long Non-Coding RNA THOR Enhances the Stem Cell-Like Traits of Triple-Negative Breast Cancer Cells Through Activating β-Catenin Signaling.

Abstract

BackgroundThe oncogenic roles of lncRNA THOR have been revealed in several tumors, however, its functions in breast cancer are still unclear.Material/MethodsReal-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.ResultsTHOR 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 β-catenin mRNA, enhanced β-catenin mRNA stability and thus increased its expression. Furthermore, overexpression of β-catenin partially diminished THOR silencing-mediated inhibition on TNBC cell stemness.ConclusionsThis work proposes that THOR facilitates TNBC cell stemness through activating β-catenin signaling.