Conclusion
The study suggested that lncRNA HCP5 might promote malignant behaviors of OC cells through the miR-525-5p/PRC1 crosstalk and the Wnt/β-catenin pathway. Silencing of HCP5 might serve as a novel option for OC treatment.
Methods
Microarray analysis was conducted to probe aberrantly expressed lncRNAs in OC tissues. Artificial silencing of lncRNA HCP5 was introduced in OC cells to identify its role in cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT). The potential downstream targets of lncRNA HCP5 were predicted by bio-information system and validated through dual luciferase reporter gene assays. Silencing of microRNA-525-5p (miR-525-5p) was introduced in cells to probe its role in cell behaviors. Xenograft tumors were induced in nude mice for in vivo experiments.
Purpose
Owing to the late diagnosis and frequent metastasis, ovarian cancer (OC) exhibits a high mortality rate. The study was intended to figure out the function of long non-coding RNA (lncRNA) HCP5 in OC metastasis.
Results
High expression of lncRNA HCP5 was found in OC tissues and cells. Silencing of lncRNA HCP5 led to a decrease in cell proliferation, invasion, migration and EMT process. LncRNA HCP5 is mainly sub-localized in cytoplasm. LncRNA HCP5 could act as a sponge for miR-525-5p, which could further bind to polycomb repressive complex 1 (PRC1). Knockdown of miR-525-5p partly recovered the biological behaviors of OC cells inhibited by HCP5 silencing. In addition, HCP5 promoted Wnt/β-catenin signaling pathway activity. Silencing of lncRNA HCP5 also impeded growth and metastasis of tumor in mice.