Conclusion
In conclusion, our research explains the mechanism of KCNQ1OT1 in OS progression, which could serve as a new therapeutic target.
Methods
Cell viability and proliferation were detected using the CCK-8 assay and the 5-Ethynyl-2'-deoxyuridine (EdU) assay. Wound-healing assays, transwell assay and flow cytometry were used to identify cell migration, invasion, and apoptosis, respectively. The relationship among KCNQ1OT1, miR-154-3p, and KLF12 was verified by luciferase reporter assay and restricting protein immunoprecipitation (RIP) assay. Xenograft models were established to confirm the function of KCNQ1OT1 in vivo.
Objective
Osteosarcoma (OS) is a common bone cancer that usually influences children. Metastasis and recurrence are the main reasons for the poor prognosis. In this study, we investigated the functions and mechanisms of KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OS.
Results
The expression of KCNQ1OT1 was higher in OS than in non-tumor tissues and cells. Knockdown of KCNQ1OT1 could reduce OS cell proliferation, migration, and invasion and promoted cell death. Mechanistically, KCNQ1OT1 contributed to OS formation by acting as a competitive endogenous RNA (ceRNA) and influencing miR-154-3p expression. Furthermore, we confirmed that miR-154-3p affected KLF12 expression through binding the 3'UTR region. Finally, rescue experiments determined that KCNQ1OT1 exerted major roles in OS through the miR-154-3p/KLF12 axis.