Journal: Scientific Reports

Article Title: Porphyromonas gingivalis promotes oral squamous cell carcinoma progression via the IL-6/EZH2/Snai2 axis

doi: 10.1038/s41598-026-41528-w

Figure Lengend Snippet: Exploration of the functions of EZH2 and Snai2 in the OSCC progressions. (A) EZH2 and Snai2 expression level in primary OSCC cells (POSCC) or normal oral epithelial cells as control (NC) before and after IL-6 treatment. (B) EZH2 and Snai2 mRNA transcription level in primary OSCC cells (POSCC) before and after IL-6 treatment. (C) Cell proliferation assay of the OSCC cell line, HSC-2, with different treatments targeting EZH2. EZH2-OE: EZH2 overexpression; EZH2-KD: EZH2 knockdown; EZH2-KD & ReEZH2: EZH2 knockdown cells with EZH2 recombinant protein rescuing management. (D) Cell migration assay of HSC-2 with different treatments targeting EZH2. The cell migration rate was monitored by RTCA analyzer and calculated as cell index. (E) mRNA transcription level of Snai2 in HSC-2 with different treatments targeting EZH2. (F) Cell proliferation assay of HSC-2 with different treatments targeting Snai2. Snai2-OE: Snai2 overexpression; Snai2-KD: Snai2 knockdown. (G) Cell migration assay of HSC-2 with different treatments targeting Snai2. Each experiment for RTCA analysis was performed with duplication of samples ( N = 2), while for other items was with triplication of samples ( N = 3) and the error bars were presented as SD result. The independent experiment was performed at least three times. For the statistic test using, results in panel B were analyzed with student’s t-test, in panel C, E and F were analyzed with One-way ANOVA method, and in D and G were with Two-way ANOVA method.

Article Snippet: Samples were blocked with 5% non-fat milk in TBST for 1 h at room temperature and incubated with the EZH2 primary antibody (1: 1000, orb1939414, biorbyt, UK) and Snai2 primary antibody (1: 1000, orb197797, biorbyt, UK) overnight at 4 °C.

Techniques: Expressing, Control, Proliferation Assay, Over Expression, Knockdown, Recombinant, Cell Migration Assay, Migration

Journal: Scientific Reports

Article Title: Porphyromonas gingivalis promotes oral squamous cell carcinoma progression via the IL-6/EZH2/Snai2 axis

doi: 10.1038/s41598-026-41528-w

Figure Lengend Snippet: Determination of the effects of EZH2 regulated Snai2 signal on OSCC progression. (A) Wound healing images (left panel) and the quantification data (right panel) of HSC-2 from 0 h to 24 h, in different groups. EZH2-OE: EZH2 overexpression; SiSnai2: SiRNA treatment targeting Snai2. (B) Cell proliferation assay of HSC-2 with different treatments. (C) Cell migration assay of HSC-2 with different treatments. The cell migration rate was monitored by RTCA analyzer and calculated as cell index. (D) Cell proliferation assay of POSCC with different treatments. POSCC: primary OSCC cells without treatment; IL-6: primary OSCC cells with IL-6 stimulation; IL-6 & inEZH2: primary OSCC cells with EZH2 inhibitor treatment after IL-6 stimulation; IL-6 & SiSnai2: primary OSCC cells with Snai2 SiRNA treatment after IL-6 stimulation. (E) Cell migration assay of POSCC with different treatments. Each experiment for RTCA analysis was performed with duplication of samples ( N = 2), while for other items was with triplication of samples ( N = 3) and the error bars were presented as SD result. The independent experiment was performed at least three times. For the statistic test using, results in panel A, B and D were analyzed with One-way ANOVA method, and in C and E were with Two-way ANOVA method.

Article Snippet: Samples were blocked with 5% non-fat milk in TBST for 1 h at room temperature and incubated with the EZH2 primary antibody (1: 1000, orb1939414, biorbyt, UK) and Snai2 primary antibody (1: 1000, orb197797, biorbyt, UK) overnight at 4 °C.

Techniques: Over Expression, Proliferation Assay, Cell Migration Assay, Migration

Journal: Scientific Reports

Article Title: Porphyromonas gingivalis promotes oral squamous cell carcinoma progression via the IL-6/EZH2/Snai2 axis

doi: 10.1038/s41598-026-41528-w

Figure Lengend Snippet: Bioinformatic analysis of relationships among Snai2, EMT, and P.g. infection. (A) GSEA enrichment of Snai2 in OSCC correlating with the terms from Biological Process (right panel), Molecular Functions (mid panel), and Cellular Structures (left panel). (B) Volcano plot of the DEGs in OSCC samples standardized to the normal samples. (C) The Kaplan–Meier (K-M) survival curve of OSCC patients with Snai2 expression. The x-axis and y-axis were pointing time and survival probability, respectively, and the high Snai2 expression group and low Snai2 expression group were illustrated as red line and blue line, respectively. D , E. Functional enrichment of the screened DEGs in KEGG database with the Benjamini & Hochberg analyzing method. Relevant signal pathways (D) and their relationships with IL-6 and Snai2 (E) were shown. F. PPI analysis of the DEGs corresponding proteins in the selected genes group from KEGG enrichment. The selected proteins were divided to two groups, the infection relevant proteins (orange) and the cancer metastasis relevant proteins (teal). The proteins IL-6, EZH2 and Snai2 were highlighted with green color.

Article Snippet: Samples were blocked with 5% non-fat milk in TBST for 1 h at room temperature and incubated with the EZH2 primary antibody (1: 1000, orb1939414, biorbyt, UK) and Snai2 primary antibody (1: 1000, orb197797, biorbyt, UK) overnight at 4 °C.

Techniques: Infection, Expressing, Functional Assay

Journal: iScience

Article Title: N6-methyladenosine modification of B7-H3 mRNA promotes the development and progression of colorectal cancer

doi: 10.1016/j.isci.2024.108956

Figure Lengend Snippet:

Article Snippet: Mouse monoclonal anti-Slug , OriGene , Cat#TA800167; RRID: AB_2625278.

Techniques: Recombinant, Software

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A The headshot and clinical images of the proband. The headshot on the top panel shows the impressive facial features of the proband. The left CT image on the bottom panel shows supernumerary teeth. The right MRI image on the bottom panel shows a conspicuous CSP (see the red arrow) between the two lateral ventricles in his brain. B Pedigree analysis of a six WS family members with SNAI2 mutations. Affected individuals are represented by filled symbols, with color coding indicating phenotypic severity: purple denotes WS-affected individuals presenting characteristic facies and dental abnormalities without ID, while red represents individuals exhibiting the complete phenotype including characteristic facies, dental abnormalities, and ID. Unaffected family members are indicated by empty symbols, and deceased individuals are denoted by slashed symbols. Individuals with undetermined WS status are marked with a question mark (?). Asterisks indicate family members selected for whole-exome sequencing analysis. C A missense substitution of c.230 C > G in SNAI2 of 8q11.21 in six members (II-1, II-3, III-1, III-4, III-5 and III-6) of this family. D Conservation analysis of SNAI2 protein sequence across species and structural characterization. The upper panel illustrates the evolutionary conservation of a SNAI2 domain among five vertebrate species: Human (Homo sapiens), Rhesus monkey (Macaca mulatta), Mouse (Mus musculus), Dog (Canis lupus familiaris), and Zebrafish (Danio rerio). Within the highlighted grey region, the amino acid residue at position 77 demonstrates species-specific variation: while human and other species maintain serine (Ser) at this position, mouse uniquely possesses threonine (Thr). The middle panel is a schematic representation of the SNAI2 protein with the S77C mutation indicated by a red dot. The bottom panel applied Swiss-Model to present the predicted structural model of the SNAI2 protein in which Ser77 is labeled.

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques: Sequencing, Residue, Mutagenesis, Labeling

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A The left panel consists of photographs of Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice, along with those of the brains from each of the groups. The bar charts on the right panel compare the body weight (g), body length (cm), brain weight (g), and the brain weight/body weight ratios of mice across the three groups (n = 28 per group, 11 males and 17 females). Data are presented as mean ± SEM. Statistical analysis was done with one-way ANOVA followed by post-hoc Tukey’s multiple comparisons. ns = not significant, *** p < 0.001. B The depigmented hair along the midline of abdominal wall and around the eye fissures of the Snai2 −/− mouse, whereas Snai2 +/+ and Snai2 +/− mice have no depigmentation of skin and hair. C The radiographic analysis comprises two imaging modalities: the first column displays X-ray images of the skull, cervical vertebrae, lumbar vertebrae, and rib cage, while the second and third columns present three-dimensional CT reconstructions of skull morphology, craniofacial bone architecture, and dental anatomy, respectively. Distinctive morphological abnormalities in Snai2 − / − mice are indicated by red arrows. These marked regions in Snai2 − / − mice exhibit significant developmental retardation and structural anomalies when compared with both Snai2 +/+ and Snai2 +/ − mice. D Kaplan-Meier survival curves comparing the lifespan of Snai2 +/+ , Snai2 +/−, and Snai2 −/− mice (n = 50 per group, with an equal number of males and females).

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques: Imaging

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A The bar charts showing results from the OF test done with Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice ( Snai2 +/+ n = 32, Snai2 +/− n = 32, Snai2 −/− n = 18). B The line chart showing results from BM test done with Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice ( Snai2 +/+ n = 10, Snai2 +/− n = 10, Snai2 −/− n = 10). C The bar charts showing results from the NOR test done with Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice ( Snai2 +/+ n = 32, Snai2 +/− n = 32, Snai2 −/− n = 18). D The line chart showing the results from the NB test done with Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice ( Snai2 +/+ n = 32, Snai2 +/− n = 32, Snai2 −/− n = 20). E Representative images of regional brain glucose metabolism measured by 18 F-FDG PET in Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice. The heat maps show differential glucose uptake in various brain regions of mice. F Standardized uptake value (SUV) of 18 F-FDG in various brain regions of Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice (n = 6 per group). Data are presented as mean ± SEM in ( A – D ), and ( F ). Each group has an equal number of males and females. Statistical analysis was done with one-way ANOVA followed by post-hoc Tukey’s multiple comparisons. ns=not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques:

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A PCA of RNA-seq data from brain tissue of Snai2 +/+ , Snai2 +/− , and Snai2 −/− mice. The black dashed-line contours delineate the approximate distribution boundaries of sample clusters according to their respective genotypes. Notably, the PCA reveals distinct transcriptional profiles, with Snai2 − / − mice forming a separate cluster that is clearly segregated from the overlapping distribution of Snai2 +/+ and Snai2 +/ − mice, indicating substantial transcriptomic differences between Snai2 − / − mice and the other two groups. B Volcano plots showing DEGs in the cerebral cortex (top), hippocampus (bottom left), and the other brain regions (bottom right) in Snai2 −/− mice relative to Snai2 +/+ mice. The down-regulated expression of c-fos is labeled. C Heatmap of selected DEGs in the cerebral cortex, hippocampus, and the other brain regions of Snai2 +/+ and Snai2 −/− mice. Gene expression levels are represented as z-scores, with red indicating up-regulated expression and blue indicating down-regulated expression. Genes of interest are labeled on the right side of the heatmap. The expressions of Snai2 and c-fos decrease significantly in the Snai2 −/− mice. D Correlation heatmap of the gene expression in Snai2 −/− mice. The heatmap shows the Pearson correlation coefficients between gene pairs, with red indicating a positive correlation and blue indicating a negative correlation. Robust positive correlations were observed between c-fos and Arl4d , Depp1 , Hspa1b , Hspa1a , as well as mt − Nd4l . E Venn diagrams showing the overlap of up-regulated (top) and down-regulated (bottom) genes in the cerebral cortex, hippocampus, and other brain regions of Snai2 −/− mice. F GO enrichment analysis of up-regulated (top) and down-regulated (bottom) genes in the cerebral cortex, hippocampus, and other brain regions of Snai2 −/− mice. Snai2 +/+ , Snai2 +/− , and Snai2 −/− (n = 12 per group). Each group has an equal number of males and females.

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques: RNA Sequencing, Expressing, Labeling, Gene Expression

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A UMAP plots and cell type composition in brain tissue of Snai2 +/+ and Snai2 −/− mice. The UMAP plots on the left panel show six cell clusters in brain tissue of Snai2 +/+ (13174 cells) and Snai2 −/− (13614 cells) mice. Each colored region represents a distinct cell type, including oligodendrocyte, neuron, others, astrocyte, progenitor cell, and endothelial cell. Black dashed-line boxes delineate significant differences in both the spatial distribution and morphological characteristics of astrocytes between Snai2 +/+ and Snai2 −/− mice. The stacked bar plots on the right panel show the proportion of each of the six cell clusters in brain tissue of Snai2 +/+ and Snai2 −/− mice. B Pseudotime analysis of astrocyte lineage in brain tissue of Snai2 +/+ and Snai2 −/− mice. The UMAP plots on the left panel show the developmental trajectory of astrocyte lineage in brain tissue of Snai2 +/+ and Snai2 −/− mice. Distinct spatial patterns were observed between genotypes: in Snai2 +/+ mice, C1 astrocytes demonstrate a more concentrated distribution pattern with broader tissue coverage compared to the relatively dispersed and restricted distribution observed in Snai2 −/− mice, as demarcated by black dashed lines. The stacked bar plots on the right panel show the proportion of each of the five astrocyte clusters in brain tissue of Snai2 +/+ and Snai2 −/− mice. The red rectangular frame highlights a significantly higher proportion of C1 astrocytes in Snai2 +/+ mice compared to Snai2 −/− mice, indicating genotype-dependent differences in astrocyte subpopulation distribution. C GSVA of metabolic processes in the five astrocyte clusters (C1-C5). The GSVA plot illustrates the metabolic processes in the five astrocyte clusters, with C1 exhibiting significantly higher enrichment scores for genes involved in acetylcholine metabolism compared to other metabolic pathways. D Pseudotime trajectory of astrocyte clusters in brain tissue of Snai2 +/+ and Snai2 −/− mice. Astrocytes in Snai2 +/+ mouse predominantly differentiate into C1 and C5 clusters, while the differentiation process almost stops at C2 thereby leading to significant decreases in C1 and C5 clusters in the Snai2 −/− mouse brain. E Box plots show the predicted ordering of cell clusters within astrocyte lineage (C1-C5) based on cellular (Cyto) trajectory reconstruction analysis using gene counts and expression (CytoTRACE) scores. Higher CytoTRACE scores indicate less differentiated cells, while the comparatively lower scores observed in C1 astrocytes indicate a more terminally differentiated cellular state.

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques: Expressing

Journal: Translational Psychiatry

Article Title: Developmental arrest of astrocyte lineage in Snai2 deletion mice: implication for the intellectual disability in patients with Waardenburg syndrome

doi: 10.1038/s41398-025-03616-9

Figure Lengend Snippet: A UMAP plots of cell clusters in brain tissue of Snai2 +/+ and Snai2 −/− mice. The UMAP plots on the left panel show 18 cell clusters in brain tissue of Snai2 +/+ (3833 cells) and Snai2 −/− (3899 cells) mice. The stacked bar plots on the right panel show proportion of each cell cluster in brain tissue of Snai2 +/+ and Snai2 −/− mice. Cell clusters are color-coded as indicated in the legend. B Spatial transcriptomic maps projected onto the same sagittal brain sections from each Snai2 +/+ and Snai2 −/− mouse. The regions of interest shown here are cerebral cortex, septum, hippocampus, amygdala, thalamus, hypothalamus, and parts of cerebellum and striatum. The mRNA expression profiles relate to 18 cell clusters from C0 to C17, including subtypes of astrocyte, endothelial cell, oligodendrocyte, progenitor cell, and others, in addition to those of neuron. The black dashed lines demarcate the anatomical boundaries of the cerebral cortex and hippocampus, corresponding to clusters C1, C5, C6, and C8 in panel A. C The stacked bar plots show different proportions of certain cell clusters in certain brain regions of Snai2 +/+ and Snai2 − / − mice. D GSVA of signaling pathways in all (C0-C17) cell clusters of the Snai2 − / − mouse brain. E Levels and spatial distribution of c-fos expression in the same sagittal brain sections from each Snai2 +/+ and Snai2 − / − mouse. The white dashed lines delineate the cerebral cortex and hippocampus, which are known to play pivotal roles in cognitive processes.

Article Snippet: Knockout C57BL/6N- Snai2 tm1cyagen mice were designed by Cyagen Biosciences (Suzhou, China).

Techniques: Expressing, Protein-Protein interactions

Journal: iScience

Article Title: N6-methyladenosine modification of B7-H3 mRNA promotes the development and progression of colorectal cancer

doi: 10.1016/j.isci.2024.108956

Figure Lengend Snippet:

Article Snippet: The primary antibodies used were anti-B7-H3 (1:400; Proteintech, Cat No. 14453-1-AP), anti-ALDH (1:100; Abcepta, Cat No. AP1465c), anti-CD133 (1:500; Abcam, Cat No. ab27699), anti-MYC (1:500; Abcam, Cat No. ab18185), anti-NANOG (1:500; Novus, Cat No. NB100-58842), anti-SOX2 (1:300; Novus, Cat No. NB110-79875), anti-Ki67 (1:200; Proteintech, Cat No. 27309-1-AP), anti-Slug (1:1000; OriGene, Cat No. TA800167), anti-N-cadherin (1:5000; Proteintech, Cat No. 22018-1-AP) and anti-E-cadherin (1:2000; OriGene, Cat No. TA800692).

Techniques: Recombinant, Software

Journal: Oncology reports

Article Title: MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer.

doi: 10.3892/or.2016.5163

Figure Lengend Snippet: Figure 3. Snail family zinc finger 2 (SNAI2) is a target of miR-21 in breast cancer. (A) Sequence alignment of human miR-124 with the 3'-untranslated region (3'‑UTR) of SNAI2. The seed sequence of miR-124 matches the 3'-UTR of SNAI2. (B) Correlation between the ratio of miR-124 expression in the breast cancer tissues compared to adjacent normal tissues and SNAI2. The r-values were calculated by Spearman correlation analysis. (C) The expression level of SNAI2 was significantly increased in breast cancer cell lines compared to MCF-10A cells. The graph displays the mean of 2-∆∆Ct value ± SEM; ***P<0.001. (D) Western blotting assay of MCF-7 cells transfected with miR-124. (E) Effect of miR-124 on SNAI2 expression as determined by a luciferase reporter assay. The data were normalized by determining the ratio of firefly and Renilla luciferase activities measured at 24-h post-transfection. The results shown represent the mean ± SEM of triplicate experiments. ***P<0.001; n.s., not significant.

Article Snippet: Short hairpin RNA (shRNA) constructs against SNAI2 were from Origene Co. (GenePharma).

Techniques: Sequencing, Expressing, Western Blot, Transfection, Luciferase, Reporter Assay

Journal: Oncology reports

Article Title: MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer.

doi: 10.3892/or.2016.5163

Figure Lengend Snippet: Figure 4. Inhibition of snail family zinc finger 2 (SNAI2) reduces tumorigenic activity in breast cancer cells. (A) Western blotting validated the downregulation of SNAI2 after short hairpin RNA (shRNA) knockdown in MCF-7 cells. (B-F) SNAI2 knockdown reduces the proliferation capacity (B), colony formation capacity (C), migration capacity (D and E) and invasion capacity (F) of MCF-7 cells. Bar graphs display mean ± SEM of triplicate experiments. **P<0.01, ***P<0.001.

Article Snippet: Short hairpin RNA (shRNA) constructs against SNAI2 were from Origene Co. (GenePharma).

Techniques: Inhibition, Activity Assay, Western Blot, shRNA, Knockdown, Migration