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

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.

• Authors: Binbin Wang, Qiang Ye, Chuantao Zou
• Journal: Medical science monitor : international medical journal of experimental and clinical research (Med Sci Monit) Vol. 26 Pg. e923507 (Jul 14 2020) ISSN: 1643-3750 [Electronic] United States
• PMID: 32665537 (Publication Type: Journal Article)

Chemical References

• CTNNB1 protein, human
• RNA, Long Noncoding
• RNA, Messenger
• beta Catenin

Topics

• Cell Line, Tumor
• Cell Proliferation (physiology)
• Female
• Gene Expression
• Humans
• Neoplastic Stem Cells (metabolism, pathology)
• RNA, Long Noncoding (genetics)
• RNA, Messenger (genetics, metabolism)
• Signal Transduction
• Triple Negative Breast Neoplasms (genetics, metabolism, pathology)
• Wnt Signaling Pathway
• beta Catenin (genetics, metabolism)