Journal: Cancer Biology & Therapy

Article Title: Centromere protein I promotes hepatocellular carcinoma progression by activating PI3K/AKT/mTOR-CDK2 cascade

doi: 10.1080/15384047.2026.2667596

Figure Lengend Snippet: Proliferation, survival, and invasion phenotypes were reshaped by gain- and loss-of-function perturbation. (A) WB analysis of CENPI protein in HCC cell lines (HCCLM3, Hep3B, and HepG2); HepG2 showed the highest CENPI expression ( n = 3). (B) WB analysis of CENPI protein in si-CENPI-transfected HepG2 cells; si-CENPI decreased CENPI levels vs si-NC, *** p < 0.001 ( n = 3). (C) WB analysis of CENPI protein in oe-CENPI-transfected HepG2 cells; oe-CENPI increased CENPI levels vs oe-NC, *** p < 0.001 ( n = 3). (D) CCK-8 assay for HepG2 proliferation; si-CENPI decreased absorbance (weaker proliferation) vs si-NC, while oe-CENPI increased it (stronger proliferation) vs oe-NC, * p < 0.05 ( n = 3). (E) Wound-healing assay for HepG2 migration; healing status recorded at 0/24 h. si-CENPI decelerated wound closure vs si-NC, while oe-CENPI accelerated it vs oe-NC; scale bar = 100 μm, ** p < 0.01 ( n = 3). (F) Flow cytometry for HepG2 apoptosis; apoptotic rates quantified. si-CENPI increased apoptotic rate vs si-NC, while oe-CENPI decreased it vs oe-NC, ** p < 0.01 ( n = 3). (G) Transwell assay for HepG2 invasion in Matrigel-coated chambers; invaded cells stained and counted. si-CENPI reduced invaded cells vs si-NC, while oe-CENPI increased them vs oe-NC; scale bar = 275 μm, *** p < 0.001 ( n = 3). (H) Flow cytometry for HepG2 cell cycle; si-CENPI increased the proportion of cells in G1 phase and decreased that in S phase vs si-NC, ** p < 0.01, while oe-CENPI showed the opposite effect vs oe-NC, * p < 0.05 ( n = 3). Data are presented as mean ± SD of three independent experiments; error bars represent SD.

Article Snippet: CENPI-targeting siRNAs and a nontargeting control siRNA (si-NC) were synthesized by Sangon Biotech (Shanghai, China).

Techniques: Expressing, Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Flow Cytometry, Transwell Assay, Staining

Journal: Cancer Biology & Therapy

Article Title: Centromere protein I promotes hepatocellular carcinoma progression by activating PI3K/AKT/mTOR-CDK2 cascade

doi: 10.1080/15384047.2026.2667596

Figure Lengend Snippet: Cell cycle and mTORC1 programs emerged as dominant signatures accompanied by CDK2 elevation and EMT marker remodeling. (A) KEGG pathway enrichment analysis (top ten significantly enriched pathways); the cell cycle pathway was most significant, with significance represented by −log10 ( p value), based on CENPI-related differentially expressed genes. (B) GSEA analysis of CENPI-related genes; enriched pathways include cell cycle-related (E2F_TARGETS) and mechanism-related (mTORC1_SIGNALING), significance represented by normalized enrichment score (NES). (C) WB analysis of cell cycle-related proteins (CDK2, Cyclin D1) and CENPI in si-CENPI and oe-CENPI-transfected HCC cells; CDK2 showed the most obvious change, ** p < 0.01 vs si-NC and * p < 0.05 vs oe-NC ( n = 3). (D) WB detection of PI3K/AKT/mTOR pathway proteins (PI3K, p-PI3K, AKT, p-AKT, mTOR, p-mTOR), EMT proteins (N-cadherin, E-cadherin, Vimentin), and CENPI in si-CENPI and oe-CENPI-transfected HCC cells, * p < 0.05 and ** p < 0.01 ( n = 3). Quantitative data are presented as mean ± SD of three independent experiments; error bars represent SD.

Article Snippet: CENPI-targeting siRNAs and a nontargeting control siRNA (si-NC) were synthesized by Sangon Biotech (Shanghai, China).

Techniques: Marker, Transfection

Journal: Cancer Biology & Therapy

Article Title: Centromere protein I promotes hepatocellular carcinoma progression by activating PI3K/AKT/mTOR-CDK2 cascade

doi: 10.1080/15384047.2026.2667596

Figure Lengend Snippet: Orthotopic growth suppression was accompanied by pathway deactivation and reversal of EMT marker directionality. (A and B) Quantification of tumor weight in orthotopic xenograft models; shRNA-mediated CENPI silencing reduced tumor weight compared with models; scale bar = 1 cm, (C) Assessment of body weight changes; CENPI silencing attenuated cachexia-driven body weight loss, *** p < 0.001 vs control and ### p < 0.001 vs model ( n = 6). (D) Measurement of final tumor mass; CENPI silencing decreased tumor mass vs models without overt hepatotoxicity, ** p < 0.01 vs model ( n = 6). (E) WB analysis of EMT markers (E-cadherin, N-cadherin, and Vimentin) and PI3K/AKT/mTOR-CDK2 pathway proteins in resected tumor tissues. CENPI silencing induced a mesenchymal-to-epithelial reverting signature, with E-cadherin increased and N-cadherin/Vimentin suppressed. Concomitantly, p-PI3K, p-AKT, p-mTOR, and total CDK2 levels were diminished, indicating inactivation of the PI3K/AKT/mTOR-CDK2 relay, * p < 0.05 vs control, # p < 0.05, and ## p < 0.01 vs model ( n = 3). Data are presented as mean ± SD; error bars represent SD.

Article Snippet: CENPI-targeting siRNAs and a nontargeting control siRNA (si-NC) were synthesized by Sangon Biotech (Shanghai, China).

Techniques: Marker, shRNA, Control