Fig. 3: CircKIF18A regulates NPC senescent phenotypes. | Experimental & Molecular Medicine

Fig. 3: CircKIF18A regulates NPC senescent phenotypes.

From: Oxidative stress-induced circKIF18A downregulation impairs MCM7-mediated anti-senescence in intervertebral disc degeneration

Fig. 3

a The CCK-8 assay showed the effects of sh-circKIF18A on NPC viability (n = 3; three different donors; *P < 0.05, **P < 0.01). b The CCK-8 assay showed the impact of circKIF18A overexpression on NPC viability (n = 3; three different donors; *P < 0.05, **P < 0.01). c CircKIF18A functions in cell proliferation, as detected using an EdU assay (n = 5, five different donors; scale bar: 50 μm). d and e CircKIF18A overexpression reduced the number of SA-β-gal-positive cells, but circKIF18A knockdown enhanced senescence in NPCs (n = 3, three different donors for three individual experiments; *P < 0.05, **P < 0.01; scale bar: 50 μm). f and g The protein levels of aggrecan, collagen II, MMP-13, and MMP-3 in NPCs with or without circKIF18A knockdown and circKIF18A overexpression were determined using western blotting (n = 3, three different donors). h Representative safranin O staining images of NPCs transfected with sh-circKIF18A or circKIF18A overexpression lentiviruses (n = 3, three different donors). i and j The qRT–PCR assay showing the mRNA expression of ACAN, COL2A1, MMP13, and MMP3 in circKIF18A-silenced and circKIF18A-overexpressing NPCs (n = 3, three different donors for three individual experiments; NS, no significance; *P < 0.05; **P < 0.01). All data are presented as the mean ± SD values.

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