Conclusion
LINC00240 knockdown restrained cell proliferation, invasion, migration, and angiogenesis, while it advanced apoptosis via miR-26a-5p in NPC by EZH2 inhibition.
Methods
MiR-26a-5p inhibitor, mimic, and siLINC00240 were transfected into NPC cells. QRT-PCR was employed to assess miR-26a-5p and LINC00240 expressions. The targeting relationship of LINC00240 and miR-26a-5p was analyzed through dual luciferase reporter and RNA immunoprecipitation assay. Cell counting kit-8 assay, colony formation assay, flow cytometry assay, wound healing assay, Transwell assay and in vitro angiogenesis assay were adopted for the evaluation of the effects of LINC00240 or miR-26a-5p and LINC00240 on NPC cells regarding cell proliferation, apoptosis and cycle, migration, invasion, and angiogenesis. EZH2, cell cycle, and epithelial-mesenchymal transition (EMT)-related protein expression was tested through Western blot.
Objective
This study intended to explore the regulatory functions of LINC00240 on nasopharyngeal carcinoma (NPC).
Results
LINC00240 had a high expression in NPC tissues and cell lines. Silenced LINC00240 significantly suppressed the 5-8F and HK1 cell proliferation, invasion, migration, and angiogenesis, but raised cell apoptosis, and cells were blocked in G0/G1 phase. MiR-26a-5p was a target of LINC00240. MiR-26a-5p upregulation suppressed the NPC cell proliferation, migration, invasion, angiogenesis, N-cadherin and EZH2 expression, while it elevated apoptosis and p21, p27 and E-cadherin expressions, whereas miR-26a-5p downregulation performed conversely. LINC00240 knockdown partially offset the effects of miR-26a-5p downregulation on cell proliferation, migration, invasion, angiogenesis, apoptosis, and EZH2.