Conclusion
CDKN2B-AS1, as a lncRNA, can regulate E2F2 by sponging miR-98-5p to promote the proliferation, clone formation, and invasion of NPC cells.
Methods
The expressions of CDKN2B-AS1, miR-98-5p, and E2F2 in NPC tissues and cell lines (SUNE-1, 5-8F, 6-10B, and HK-1) as well as in peritumoral normal tissues and cell line NP69 were determined by qRT-PCR. Subcellular localization of CDKN2B-AS1 was detected using the fluorescence in situ hybridization assay. The targeting relationships between CDKN2B-AS1 and miR-98-5p as well as between miR-98-5p and E2F2 were analyzed by the dual-luciferase reporter assay and RNA binding protein immunoprecipitation assay. The proliferation, clone formation and invasion of 5-8F cells were measured using the CCK-8 assay, Clone formation assay, and transwell assay, respectively.
Objective
To explore the effect of CDKN2B antisense RNA 1 (CDKN2B-AS1) on the proliferation, clone formation, and invasion of nasopharyngeal carcinoma (NPC) cells by regulating miR-98-5p/E2F transcription factor 2 (E2F2) axis.
Results
CDKN2B-AS1 was highly expressed in NPC tissues and cells, whereas the expression of miR-98-5p decreased in the NPC tissues and cells. Silencing of CDKN2B-AS1 inhibited the proliferation, clone formation, and invasion of NPC cells (all P<0.05). CDKN2B-AS1 acted asceRNA of miR-98-5p, and miR-98-5p inhibitor could partially reverse the inhibitory effect of silencing CDKN2B-AS1 on NPC cells (all P<0.05). CDKN2B-AS1 upregulated E2F2 by inhibiting miR-98-5p, and the upregulation of E2F2 partially reversed the inhibitory effect of miR-98-5p overexpression on the NPC cells (all P<0.05).