Journal: Cancer Communications

Article Title: CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer

doi: 10.34133/cancomm.0016

Figure Lengend Snippet: CEBPB regulates gastric plasticity through its global enhancer-binding function. (A) H3K27ac modification levels, chromosomal accessibility (defined by ATAC-seq signals), and the number of CEBPB-binding sites across the genome in the NCI-N87 ( n = 2). (B) CEBPB Cut&Tag, H3K27ac Cut&Tag, and ATAC-seq peak signal levels flanking ±5 kb of the CEBPB binding sites (indicated by the black box) in NCI-N87 ( n = 2). (C) Venn diagrams showing the overlap between putative enhancers and CEBPB binding sites. (D) Gene set enrichment analysis of malignant and nonmalignant cell clusters using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (E) Gene set enrichment analysis of transcriptome profiles of GC cell lines derived from GCLM (red) and primary GC tissues (blue) using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (F) Gene set enrichment analysis of transcriptome profiles of CTCs using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (G to I) Expression levels of liver-specific genes ( SLC27A5 , F12 , and DECR2 ) in malignant and nonmalignant cells (G), CTCs (H), and GC cell lines (I). (J) ATAC-seq, H3K27ac Cut&Tag, and CEBPB Cut&Tag signal levels, along with putative enhancer and CEBPB binding regions, in the gene regions of SLC27A5 , F12 , and DECR2 in NCI-N87 ( n = 2). Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: ATAC-seq, assay for transposase-accessible chromatin using sequencing; CEBPB, CCAAT enhancer-binding protein beta; CPM, counts per million; Cut&Tag, cleavage under targets and tagmentation; CTC, circulating tumor cell; CTC-LM, CTC associated with liver metastasis; CTC-N, CTC not associated with liver metastasis; DECR2, 2,4-dienoyl-CoA reductase 2; F12, coagulation factor XII; GC, gastric cancer; GCLM, gastric cancer liver metastasis; Mag, malignant; Rep, replicate; SLC27A5, solute carrier family 27 member 5; TPM, transcripts per million.

Article Snippet: The cells were incubated overnight with primary antibodies anti-CEBPB (Cat. #23431-1-AP, Proteintech), anti-H3K27ac (Cat. #13-0059, EpiCypher), and IgG negative control (Cat. #13-0047, EpiCypher).

Techniques: Binding Assay, Modification, Derivative Assay, Expressing, Sequencing, Coagulation

Journal: Cancer Communications

Article Title: CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer

doi: 10.34133/cancomm.0016

Figure Lengend Snippet: Cebpb-regulated gastric plasticity evades CD8 + T cell surveillance by CD155–TIGIT interaction in vivo. (A) Schematic of in vivo mouse experiments to determine the immune-regulatory role of Cebpb ( n = 5 for each group). The healthy control group denoted the group without cancer cell transplantation, and the NC group denoted the group transplanted with MFC. (B) Tumor volume of liver metastases inferred from in vivo bioluminescence imaging results performed every 7 days from day 3 to day 50 (left) since cell transplantation, and liver metastases visualized using a bioluminescence imaging system on day 50 (right). (C) Representative H&E staining and immunohistochemistry results for Cebpb in liver metastasis tissues from the control group, MFC Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Arrows denote the representative areas of GC liver metastasis within the hepatic tissue. (D) Levels of IFN-γ, TNF-α, and the proportion of CD8 + T cells and NK cells among CD45 + immune cells in the healthy control group (green), MFC control group (gray), Cebpb-OE group (red), and Cebpb-OE plus anti-TIGIT mAbs treatment group (blue). (E) Multiplex immunofluorescence showing CD8 (green), IFN-γ (red), and nuclei (blue) in the MFC control group, Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Data were presented as the mean ± standard deviation. Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: Cebpb, CCAAT enhancer binding protein beta; H&E, hematoxylin and eosin; IFN-γ, interferon-gamma; mAb, monoclonal antibody; NC, negative control; OE, overexpression; TNF-α, tumor necrosis factor alpha; TIGIT, T cell immunoreceptor with Ig and ITIM domains.

Article Snippet: The cells were incubated overnight with primary antibodies anti-CEBPB (Cat. #23431-1-AP, Proteintech), anti-H3K27ac (Cat. #13-0059, EpiCypher), and IgG negative control (Cat. #13-0047, EpiCypher).

Techniques: In Vivo, Control, Transplantation Assay, Imaging, Staining, Immunohistochemistry, Multiplex Assay, Immunofluorescence, Standard Deviation, Binding Assay, Negative Control, Over Expression

Journal: The FASEB Journal

Article Title: Maternal Fructose Intake During Pregnancy Induced the Hepatic Glucose Homeostasis Imbalance in the Offspring by Inhibiting Glucokinase

doi: 10.1096/fj.202503081R

Figure Lengend Snippet: C/EBPβ promoted DNMT3B expression through transcriptional activation. (A) The results of PROMO database prediction. (B, C) Effects of maternal fructose intake during pregnancy on the C/EBPβ expression in the liver of offspring at 0 days and 4 weeks. Actin was used as a loading control ( n = 4 offspring samples per group). (D) Knockdown of C/EBPβ inhibited DNMT3B expression at the protein level in AML12 cells. Actin was used as a loading control ( n = 3 samples per group). (E) Dual‐Luciferase Assay revealed that C/EBPβ trans‐activates the Dnmt3b promoter ( n = 6 samples per group). (F) CHIP‐PCR results showed that C/EBPβ bound to the Dnmt3b promoter. All data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, and **** p < 0.0001.

Article Snippet: The primary antibodies used were as follows: GK (Abclonal, A15059, 1:1000), DNMT3B (Abclonal, A22658, 1:5000), HK2 (Proteintech, 22029‐1‐AP, 1:1500), GLUT2 (Proteintech, 20436‐1‐AP, 1:1500), KHK (Proteintech, 15681‐1‐AP, 1:1000), ALDOB (Proteintech, 18065‐1‐AP, 1:5000), ACLY (Proteintech, 15421‐1‐AP, 1:1000), Actin (Bioworld, BS6007M, 1:5000), and C/EBPβ (Proteintech, 23 431‐1‐AP, 1:15,000).

Techniques: Expressing, Activation Assay, Control, Knockdown, Luciferase

Journal: The FASEB Journal

Article Title: Maternal Fructose Intake During Pregnancy Induced the Hepatic Glucose Homeostasis Imbalance in the Offspring by Inhibiting Glucokinase

doi: 10.1096/fj.202503081R

Figure Lengend Snippet: Schematic diagram of the core mechanisms. The study demonstrated that maternal fructose intake during pregnancy led to glucose intolerance and insulin resistance in offspring. The abnormal hepatic glucose metabolism in offspring was associated with decreased GK expression, which was inhibited by DNMT3B. Besides, the expression of DNMT3B was regulated by C/EBPβ at the transcriptional level. This condition was improved by the administration of dorzagliatin.

Article Snippet: The primary antibodies used were as follows: GK (Abclonal, A15059, 1:1000), DNMT3B (Abclonal, A22658, 1:5000), HK2 (Proteintech, 22029‐1‐AP, 1:1500), GLUT2 (Proteintech, 20436‐1‐AP, 1:1500), KHK (Proteintech, 15681‐1‐AP, 1:1000), ALDOB (Proteintech, 18065‐1‐AP, 1:5000), ACLY (Proteintech, 15421‐1‐AP, 1:1000), Actin (Bioworld, BS6007M, 1:5000), and C/EBPβ (Proteintech, 23 431‐1‐AP, 1:15,000).

Techniques: Expressing