Fig 2: Cep55 knockdown caused activation of SAC in MI-arrested oocytes.After microinjection of Cep55 siRNA or control siRNA, the oocytes were placed in M16 containing IBMX for 24 h, then washed 9 times and transferred into IBMX-free M16 medium for 9.5 h. Bub3 (green) was localized at the kinetochores in the Cep55 si-group, while in the control group, Bub3 was dissociated from kinetochores of separating homologous chromosomes (red).

Fig 3: High expression of miR‐144‐3p exerts inhibitory effects on cervical cancer tumorigenesis. A, Putative miRNAs that might regulate CEP55. The 4 ellipses indicate prediction results from 4 databases, and the middle part represents the intersection. B, Expression of miR‐144‐3p was determined by RT‐qPCR in normal cervical epithelial cell line End1/E6E7, and cervical cancer cell lines, HeLa, CaSki, SiHa and ME180, (on the right side) as well as cervical cancer and adjacent normal tissues (on the left side), relative to U6. C, SiHa cell migration and invasion were detected by Transwell assay (scale bar = 50 µm). D, SiHa cell proliferation was detected by EdU assay (scale bar = 25 µm). E, Colony formation of SiHa cells was detected by colony formation assay. F, SiHa cell apoptosis was detected by flow cytometry. G, Representative Western blots of CDK4, Cyclin D1, E‐cadherin, Vimentin, Bcl‐2 and Bax proteins and their quantitation in SiHa cells, normalized to GAPDH. Data comparisons were analysed by an independent sample t test between two groups and by one‐way ANOVA among multiple groups, followed by Tukey's test. *P < 0.05 versus SiHa cells treated with NC. # P < 0.05 versus SiHa cells treated with sh‐NC. Data are shown as the mean ± standard deviation of three technical replicates

Fig 4: miR‐144‐3p can be transferred into cervical cancer cells by EVs derived from hBMSCs. A, Expression of miR‐144‐3p was determined by RT‐qPCR in cells, relative to U6. B, miR‐144‐3p‐Cy3 in hBMSCs and cervical cancer cells under the fluorescence microscope (scale bar = 20 µm). C, Expressions of miR‐144‐3p and CEP55 were determined by RT‐qPCR in cells, relative to U6 and GAPDH, respectively. D, Representative Western blots of CEP55 protein and its quantitation in cells, normalized to GAPDH. Data comparison was analysed by independent sample t test between two groups and by one‐way ANOVA among multiple groups, followed by Tukey's test. *P < 0.05 versus hBMSCs treated with miR‐NC or NC. # P < 0.05 versus EVs treated with NC. Data are shown as the mean ± standard deviation of three technical replicates

Fig 5: CEP55 activated NF-κB signalling. (a) Gene set enrichment analysis (GSEA) plot indicating a significant correlation between the CEP55 gene expression level and nuclear factor kappaB (NF-κB)-activated gene signatures (JAIN_NF-κB_SIGNALING). (b) Luciferase-reported NF-κB activity in SW1990 and Capan-1 cells transduced with CEP55 or shCEP55. (c) Changes in mRNA expression of NF-κB downstream targets (MYC, CCND1, BCLXL, MMP9, TWIST, VEGFC and IL6) in the indicated cells assessed by real-time PCR. (d) Changes in protein expression of NF-κB downstream targets (C-Myc, Cyclin D1 and BCLXL) in the indicated cells assessed by western blot. (e) Western blotting analysis of p-IKKβ, IKKβ, and IκBα expression in SW1990 and Capan-1 cells transduced with CEP55 or shCEP55. (f) The endogenous NF-κB activity in the indicated cells detected by an electrophoretic mobility shift assay (EMSA). The Oct-1-DNA complex served as a control.