Fig 2: RPL15 silencing inhibited HCC cells migration and invasion. A Wound-healing assay indicated that RPL15 silencing reduced HCCLM3 cell migration while RPL15 overexpression enhanced Hep3B cell migration. B Transwell assay revealed that RPL15 knockdown decreased the invasion capability of HCCLM3 cells while overexpression of RPL15 in Hep3B cells demonstrated the opposite effect. C The expressions of EMT-related genes were detected after RPL15 was silenced or overexpressed in HCC cells via western blot. Data are presented as the mean ± SD, n = 3; *P < 0.05, compared to the control group

Fig 3: Chest blast exposure changed the expression of cell adhesion proteins in the brain. (A) Western blot images of differentially expressed proteins after chest blast exposure. The expression levels of (B) Rpl15, (C) Cldn3, (D) Dmd, (E) Fmr1, (F) Glrb, and (G) Sez6 with normalized to internal control GAPDH. All experiments were repeated at least three times. All data were expressed as mean ± SEM (n = 5) and analyzed by a one-way ANOVA, followed by Tukey’s test for multiple comparisons. Differences were considered statistically significant at p < 0.05 for all analyses. ∗p < 0.05 vs. control group.

Fig 4: RPL15 involved in RPs-MDM2-p53 signaling pathway. A Western blot analysis revealed that the levels of p21 and p53 were significantly increased in HCCLM3 cells with RPL15 knockdown. B Western blotting from 0–8 h after cycloheximide (CHX) treatment to stop protein synthesis showed more stability of p53 in HCCLM3 cells with RPL15 knockdown. C RPL15 silencing suppressed the interaction of MDM2 with p53, the binding was determined by immunoprecipitation. D Effect of RPL15 on the binding of MDM2 with RPL11 and RPL5 was determined by immunoprecipitation, RPL15 silencing suppressed the interaction

Fig 5: RPL15 knockdown blocked cell cycle progression in HCC cells. A RPL15 knockdown in HCCLM3 cells induced the cell cycle arrest in G1 phase while RPL15 overexpression in Hep3B cells induced the converse effects. B Western blot analysis revealed that RPL15 silencing decreased CDK2 and Cyclin E1 expressions, while RPL15 overexpression promoted their expressions. Data are presented as the mean ± SD, n = 3; *P < 0.05, compared to the control group