Conclusions
Our study uncovered the cancer-promoting role of LINC00665 in OS, and the feedback loop of LINC00665/miR-1249-5p/WNT2B/Wnt might be a potential target for OS treatment.
Methods
Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to analyze LINC00665 expression in OS cells. Cell function assays assessed the impacts of LINC00665 on OS cell phenotype. Immunofluorescence and western blot analyzed the function of LINC00665 on epithelial-mesenchymal transition (EMT) in OS. Moreover, mechanistic assays analyzed the downstream mechanism of LINC00665 in OS cells.
Results
LINC00665 was significantly up-regulated in OS cells. LINC00665 silence facilitated OS cell proliferation, migration, invasion, and EMT while inhibiting cell apoptosis. Mechanically, LINC00665 acted as a competing endogenous RNA (ceRNA) to sponge miR-1249-5p and thereby modulated Wnt family member 2B (WNT2B) to activate Wnt pathway. Wnt pathway activated LINC00665 expression transcriptionally. Conclusions: Our study uncovered the cancer-promoting role of LINC00665 in OS, and the feedback loop of LINC00665/miR-1249-5p/WNT2B/Wnt might be a potential target for OS treatment.