Transcription factor ZNF703 activates linc-UBC1 to stimulate the progression of glioma.

OBJECTIVE: To investigate the role of the transcription factor Zinc finger 703 (ZNF703) in influencing the progression of glioma by regulating linc-UBC1 level. MATERIALS AND METHODS: Linc-UBC1 level in glioma with different staging and tumor sizes was determined. The potential influences of linc-UBC1 on viability, cell cycle progression, and invasiveness of glioma cells were evaluated. Through RNA binding protein immunoprecipitation (RIP) assay and Dual-Luciferase reporter gene assay, the interaction between ZNF703 and linc-UBC1 was assessed. The rescue experiments were conducted to identify the role of ZNF703 in regulating cellular performances of glioma by interacting with linc-UBC1. RESULTS: Linc-UBC1 was highly expressed in glioma. Its level was higher in glioma with larger tumor size or advanced staging. The knockdown of linc-UBC1 reduced viability, arrested cell cycle in the G0/G1 phase, and attenuated invasiveness of U87 and LN229 cells. The presence of the binding sites was observed in the promoter regions of ZNF703 and linc-UBC1. The overexpression of ZNF703 could alleviate the inhibited proliferative and invasive potentials in U87 and LN229 cells with the linc-UBC1 knockdown. CONCLUSIONS: The transcription factor ZNF703 promotes the proliferative and invasive potentials in glioma cells by regulating the transcriptional activity of linc-UBC1.