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. 2020 Nov 1;24(23):13813–13823. doi: 10.1111/jcmm.15971

Figure 5.

Figure 5

miR‐338‐3p inhibited USP15 function by binding to its 3′UTR. A, miR‐338‐3p was down‐regulated in degenerative NP cells. ***P < .001 vs normal. B, An miR‐338‐3p mimic inhibited apoptosis of degenerative NP cells. ***P < .001 vs NC. C, The relative mRNA level of USP15 was down‐regulated in degenerative NP cells transfected with miR‐338‐3p mimic. ***P < .001 vs NC. D, miR‐338‐3P mimic promoted the phosphorylation of AKT in degenerative NP cells. E, The knockdown of USP15 decreased the apoptosis of degenerative NP cells transfected with the miR‐338‐3p inhibitor. **P < .01 vs NC, ***P < .001 vs NC; ### P < .001 vs Inhibitor. F, Dual‐luciferase assays were performed to examine the association between miR‐338‐3p and USP15 in degenerative NP cells. The wild‐type 3′‐UTR of USP15 was cloned into luciferase reporter vectors. Then, degenerative NP cells were transfected with NC, miR‐338‐3p mimics or inhibitor in addition to a recombinant luciferase reporter vector and incubated for 48 h. ***P < .001 vs NC. G, The relative protein levels of USP15, p‐AKT and AKT were examined in NC‐, miR‐338‐3p inhibitor‐, NC + siUSP15‐, miR‐338‐3p inhibitor + siUSP15‐transfected cells. ***P < .001 vs NC; ### P < .001 vs inhibitor