Aim
To determine the role and underlying mechanism of lncRNA HCP5 in nasopharyngeal carcinoma (NPC). Method: The expression of HCP5 and miR-128-3p was assessed by qRT-PCR. CCK-8, EdU staining, and transwell were performed to determine cell progression. A nude mouse xenograft tumor model was carried out to detect the role of HCP5 in vivo. The luciferase assay was performed to confirm the function between lncRNA HCP5 and miR-128-3p.
Conclusion
lncRNA HCP5 could regulate NPC cell progression via sponging miR-128-3p, which might serve as a potential therapy target of NPC.
Results
The increased level of HCP5 was observed in NPC tissues. Silencing of HCP5 prevented tumor progression in vitro and in vivo. The luciferase assay verified that HCP5 could bind with miR-128-3p. Furthermore, forced expression of miR-128-3p could prevent the function of HCP5 on NPC cells.