Journal: Clinical Science (London, England : 1979)

Article Title: In vivo inhibition of TDO2 in fibroids results in widespread alteration in the tumor transcriptome

doi: 10.1042/CS20260395

Figure Lengend Snippet: Effects of TDO2 silencing in primary LSMC. Cells were transfected with siTDO2 or control siRNA (siNC) for 96 h, followed by assessment of gene expression by qRT-PCR. Expression levels of TDO2, VDR, MMP11, MMP14, COL11A1, CBX4, LINC02568, LINC01310, LINC02544, LINC02182, and miR-584-5p are shown. Data represent mean ± SEM from four independent experiments ( n = 4). Statistical significance is indicated as * P <0.05 and *** P <0.01.

Article Snippet: For gene silencing experiments, primary LSMCs were transfected with 50 nM of either a non-targeting control siRNA (siNC) or siRNA targeting TDO2 (siTDO2; 5′-CUAUCACUACCUGCGAUCAACUGUG-3′) using PureFection transfection reagent (System Biosciences, Mountain View, CA, U.S.A.), according to the manufacturer’s protocol.

Techniques: Transfection, Control, Gene Expression, Quantitative RT-PCR, Expressing

Journal: Bioscience Reports

Article Title: G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs

doi: 10.1042/BSR20250290

Figure Lengend Snippet: ( A, B ) G3BP1 was transiently silenced with siRNA, or not; cells were then serum-starved and stimulated with PDGF-BB, as indicated. Activation of PDGFR, STAT1, ERK1/2, AKT, PLCγ, and STAT3 signaling pathways was determined by immunoblotting for phosphorylated and total amounts of the signaling proteins. The experiments were repeated four times.

Article Snippet: AG01523 cells were transiently transfected with 20 nM siRNA of Trilencer-27 G3BP siRNA (#SR, OriGene Technologies, U.S.A.) or 20 nM scrambled negative control siRNA (#SR30004, OriGene Technologies, U.S.A.), using SilentFect reagent (Bio-Rad), and incubated for 72 to 96 h at 37°C in a CO 2 incubator.

Techniques: Activation Assay, Protein-Protein interactions, Western Blot

Journal: Bioscience Reports

Article Title: G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs

doi: 10.1042/BSR20250290

Figure Lengend Snippet: (A–F) After transient silencing of G3BP1 with siRNA, or not, and serum starvation overnight, AG01523 cells were stimulated with PDGF-BB for 1 h (black bars) or left unstimulated (0 h, gray bars). mRNA expression of G3BP1 ( A ), STAT3 ( B ), STAT1 ( C ), FOS ( D ), MYC ( E ), and CCND1 (cyclin D1) ( F ) is presented relative to the expression of control gene HPRT . Statistical analysis was performed on four independent repeats using Student’s t -test. *, P- value <0.05; **, P <0.01. The experiments were repeated six times.

Article Snippet: AG01523 cells were transiently transfected with 20 nM siRNA of Trilencer-27 G3BP siRNA (#SR, OriGene Technologies, U.S.A.) or 20 nM scrambled negative control siRNA (#SR30004, OriGene Technologies, U.S.A.), using SilentFect reagent (Bio-Rad), and incubated for 72 to 96 h at 37°C in a CO 2 incubator.

Techniques: Expressing, Control

Journal: Bioscience Reports

Article Title: G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs

doi: 10.1042/BSR20250290

Figure Lengend Snippet: ( A ) G3BP1 was knocked down by siRNA, or not, in AG01523 fibroblasts. Cells were then grown in medium containing 1% FBS and increasing concentrations of PDGF-BB. The amount of DNA and, therefore, the proliferation rate was determined by measuring absorption of fluorescently labeled DNA-intercalating dye using the CyQuant assay. The experiments were repeated three times. ( B ) Schematic illustration of the findings of the study. G3BP1 acts as a co-activator of PDGF-BB-induced activation of STAT3 and as a co-repressor of the transcription of cyclin D1 and STAT1 due to its association with the SWI/SNF chromatin remodeling complex.

Article Snippet: AG01523 cells were transiently transfected with 20 nM siRNA of Trilencer-27 G3BP siRNA (#SR, OriGene Technologies, U.S.A.) or 20 nM scrambled negative control siRNA (#SR30004, OriGene Technologies, U.S.A.), using SilentFect reagent (Bio-Rad), and incubated for 72 to 96 h at 37°C in a CO 2 incubator.

Techniques: Labeling, CyQUANT Assay, Activation Assay

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