Hsa_circ_001193 regulates proliferation and apoptosis of nasopharyngeal carcinoma cells through targeting mir-496

OBJECTIVE: To explore the effects of hsa_circ_001193 on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells. MATERIALS AND METHODS: The messenger ribonucleic acid (mRNA) expression level of hsa_circ_001193 in three NPC cell lines (CNE1, SUNS-1, and HONE-1) and human normal nasopharyngeal epithelial cell line (NP69) was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The expression of hsa_circ_001193 was silenced through transient transfection with small-interfering RNA (siRNA). Regulatory effects of hsa_circ_001193 knockdown on the proliferation and apoptosis of HONE-1 cells were determined using cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry. Potential miRNAs binding hsa_circ_001193 were predicted in the StarBase, which was further verified via Dual-Luciferase reporter assay and qRT-PCR. Moreover, the involvement of the predicted target miRNA in the proliferation of HONE-1 cells regulated by hsa_circ_001193 was determined by CCK-8 assay. RESULTS: Compared with that in human normal nasopharyngeal epithelial cell line (NP69), the expression of hsa_circ_001193 was significantly upregulated in NPC cell lines (p<0.05). The results of CCK-8 assay and colony formation assay showed that knockdown of hsa_ circ_001193 could significantly suppress the cell proliferation ability and colony formation ability compared with control group (p<0.05). The results of flow cytometry revealed that the apoptosis rate in hsa_circ_001193 knockdown group was remarkably higher than that in control group (p<0.05). Besides, according to the analysis of StarBase database, there were binding sites between hsa_circ_001193 and miR-496. The Dual-Luciferase reporter assay manifested that miR-496 bound hsa_circ_001193 (p<0.05). CONCLUSIONS: Hsa_circ_001193 can serve as the miR-496 sponge, which regulates proliferation and apoptosis of NPC cells through up-regulating miR-496. Our findings provide a new therapeutic target for NPC.