Background
Breast cancer (BC) is one of the most prevalent malignancies among women globally. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are associated with BC carcinogenesis. In the current study, we explored the mechanism by which LINC00662 regulates BC.
Conclusion
LINC00662 enhances cell proliferation, migration, invasion and stemness in BC by targeting miR-144-3p/SOX2 axis. The findings in the present study suggested that LINC00662 could be a potential therapeutic target for BC treatment.
Methods
Quantitative real-time PCR (qRT-PCR) assessed RNA expressions while western blot for protein levels. Kaplan Meier analysis evaluated overall survival (OS). Cytoplasmic/nuclear fractionation, RNA binding protein immunoprecipitation (RIP) and luciferase reporter assays probed into the underlying molecular mechanism of LINC00662 in BC. Xenograft model was established to explore the influence of LINC00662 on BC progression in vivo. R square graphs were utilized to represent RNA relationships.
Results
LINC00662 is overtly overexpressed in BC tissues and cell lines. LINC00662 knockdown hampers cell proliferation, migration, invasion and stemness. LINC00662 expression is negatively correlated with OS of BC patients. LINC00662 up-regulates SOX2 expression by competitively binding to miR-144-3p, thereby modulating BC cell progression. Xenograft experiments verified that LINC00662 promotes BC tumor growth and cell stemness in vivo.