Abstract: Objective To investigate the role and possible mechanism of CELF1 in the proliferation of glioma cells. Methods  CELF1 mRNA and protein expression in glioma cell lines U87， U251， SHG44 and human normal astrocyte line HA1800 was detected by fluorescence quantitative PCR （QPCR） and Western blotting. U87 cells were transfected with nonsense nucleic acid NC （NC group）， siCELF1 （siCELF1 group） and siCELF1＆siCDKN1B （siCELF1＆siCDKN1B group）. Cell viability was detected by CCK-8 assay， and cell cycle changes were detected by flow cytometry. The protein expression of CELF1， CDKN1B and Cyclin D1 was detected by Western blotting. Results The relative expression levels of CELF1 mRNA in glioma cell lines U87， U25 1 and SHG44 were 3.1±0.074， 4.2±0.137 and 3.6±0.023， respectively， which were higher than those in normal astrocyte line HA 1800， and the differences were statistically significant （P＜0.05）. The protein expression of CELF1 detected by Western blotting was consistent with that of mRNA. Silence CELF1 can significantly reduce U87 cell viability. The proportion of G0／G1 phase cells in siCELF1 group was （63.5±1.33）％， significantly higher than that in NC group （39.4±1.24）％；while proportion of S phase cells in siCELF1 group was （14.3±0.095）％， significantly lower than that in NC group （22.8±1.97）％ （P＜0.05）. The relative expression of CDKN1B protein in group siCELF1 was 2.37±0.088， which was significantly lower than that in NC group （P＜0.05）. The relative expression of Cyclin D1 protein in group siCELF1 was 0.274±0.039， which was significantly lower than that in siCELF1＆siCDKN1B group （P＜0.05）. Cell viability in group siCELF1＆siCDKN1B was higher than that in group siCELF1 （P＜0.05）. The proportion of G0／G1 phase cells in siCELF1-siCDKN1B group was （42.1±1.76）％， significantly lower than that in siCELF1 group （62.4±1.92）％ （P＜0.05）， while the proportion of S phase cells in siCELF1-siCDKN1B group was （20.3±0.077）％， which was not significantly different from that in NC group （22.8±1.97）％. Conclusion CELF1 mediates the expression of Cyclin D1 by inhibiting CDKN1B， and promotes glioma proliferation.

Key words: Glioma, CELF1, CDKN1B, Cyclin D1, Proliferation