Fig 1: Endogenous CENP-B and CENP-I extend further than the CENP-A domain on TEEN fibers. Representative images of chromatin fibers prepared from U2OS cells using the TEEN buffer and stained for CENP-A and either CENP-B (a) or CENP-I (b). Scale bar: 2.5 μm. Intensity plots for CENP-A and CENP-B or CENP-I gray values along the length of the fiber (in μm) are shown on the right. c Scatter plot depicting the distance of spreading from the edges of the CENP-A domain for CENP-C, CENP-H, CENP-T, CENP-B and CENP-I. Each fiber is represented by two dots, for the distance of spreading left and right of the centromere domain. Error bars represent mean with SD. FDR adjusted Kolmogorov–Smirnov p values < 0.001 are represented as **. Not significant p values > 0.05 are not depicted. n = 142 fibers for CENP-B (from three experiments), 160 fibers for CENP-C (from two experiments), 189 fibers for CENP-H (from two experiments), 177 fibers for CENP-I (from two experiments) and 142 fibers for CENP-T (from two experiments)
Fig 2: Identification of the association between hub gene and CRPC clinical characteristics. (a) Association of MCM4, CENPI, and KNTC1 expression levels with Gleason scores in CRPC samples. (b) Association of MCM4, CENPI, and KNTC1 expression levels with PSA levels in CRPC patients. (c) Association of MCM4, CENPI, and KNTC1 expression levels with NEPC scores in CRPC patients. P values were obtained by Spearman correlation analysis. All data are represented by mean ± SD.
Fig 3: Gene set enrichment analysis (GSEA) of KEGG pathway gene sets in hub genes high-expression versus low-high-expression samples from SU2C/PCF Dream Team dataset. (a–c) Top 3 gene sets (according to GSEA normalized enrichment score) enriched in the high-expression group of each hub gene. (a) MCM4; (b) CENPI; (c) KNTC1. NOM P value and FDR are shown in each plot. (d) The top 5 most related genes of each hub gene. P values were obtained by Spearman or Pearson correlation analysis.
Fig 4: (A) CCK-8 cell proliferation assay. (B) TUNEL assay of MKN28 cells treated with 20 mg/L CDDP for 24 h. (C) Cell apoptosis measured by TUNEL assay of MKN28 cells. (D) Cell apoptosis measured by flow cytometry of MKN45 cells. (E) Transwell cell migration assay of gastric cancer (GC) cells. (F) Expression of epithelial–mesenchymal transition (EMT) markers and AKT by western blotting in GC cells. (G) Centromere protein I (CENP-I) promoter methylation level and (H) CENP-I expression level in TP53-mutant and nonmutant groups in GC tissues from UALCAN database. (I) CENP-I promoter methylation levels between gender groups in GC tissues from UALCAN database.
Fig 5: (A) Centromere protein I (CENP-I) mRNA expression elevated in gastric cancer (GC) tissues compared to normal gastric tissues (P<0.0001) from UALCAN database. (B) real-time quantitative polymerase chain reaction (RT-qPCR) revealed significantly higher CENP-I mRNA expression in 40 GC tissues than that in 40 paired normal gastric tissues (P<.0001). (C) Representative images of immunohistochemical staining for CENP-I in GC and normal gastric tissues. (D) CENP-I mRNA abundance in 3 GC cell lines measured by quantitative real-time PCR (qRT-PCR). (E) CENP-I protein expression in 3 GC cell lines measured by western blotting. (F) Western blotting showed knockdown and overexpression of CENP-I in 3 GC cell lines.
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