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ATCC human oscc cell lines scc4

Expression landscape of GSDMB across different groups (330 <t>OSCC</t> tissues, 32 normal tissues). A - C Differential expression of GSDMB among Grade categories, age groups, and N stages. D Boxplot showing the expression difference of GSDMB between OSCC cases and controls. E Receiver Operating Characteristic (ROC) curve for GSDMB. F Forest plot from univariate Cox regression analysis based on GSDMB expression levels and prognostic outcomes across various cancers. G Boxplot illustrating differences in GSDMB expression between control and disease groups across pan-cancer samples. “wilcox.test” is used to calculate the significance p-value (* p<0.05, ** p<0.01, *** p<0.001)

Human Oscc Cell Lines Scc4, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 767 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human oscc cell lines scc4 - by Bioz Stars, 2026-03

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1) Product Images from "Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis"

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

Journal: BMC Oral Health

doi: 10.1186/s12903-026-07781-1

Expression landscape of GSDMB across different groups (330 OSCC tissues, 32 normal tissues). A - C Differential expression of GSDMB among Grade categories, age groups, and N stages. D Boxplot showing the expression difference of GSDMB between OSCC cases and controls. E Receiver Operating Characteristic (ROC) curve for GSDMB. F Forest plot from univariate Cox regression analysis based on GSDMB expression levels and prognostic outcomes across various cancers. G Boxplot illustrating differences in GSDMB expression between control and disease groups across pan-cancer samples. “wilcox.test” is used to calculate the significance p-value (* p<0.05, ** p<0.01, *** p<0.001)

Figure Legend Snippet: Expression landscape of GSDMB across different groups (330 OSCC tissues, 32 normal tissues). A - C Differential expression of GSDMB among Grade categories, age groups, and N stages. D Boxplot showing the expression difference of GSDMB between OSCC cases and controls. E Receiver Operating Characteristic (ROC) curve for GSDMB. F Forest plot from univariate Cox regression analysis based on GSDMB expression levels and prognostic outcomes across various cancers. G Boxplot illustrating differences in GSDMB expression between control and disease groups across pan-cancer samples. “wilcox.test” is used to calculate the significance p-value (* p<0.05, ** p<0.01, *** p<0.001)

Techniques Used: Expressing, Quantitative Proteomics, Control

Landscape of Tumor Mutational Burden (TMB) in high and low GSDMB expression groups (318 OSCC tissues). A - B Waterfall plots depicting mutations in high and low GSDMB expression groups. C Boxplot comparing TMB differences between the two groups. D Scatter plot of the correlation between TMB and GSDMB expression levels. E Kaplan-Meier survival curves for high and low TMB groups. F KM survival curves for four sample groups classified by combined TMB and GSDMB expression levels

Figure Legend Snippet: Landscape of Tumor Mutational Burden (TMB) in high and low GSDMB expression groups (318 OSCC tissues). A - B Waterfall plots depicting mutations in high and low GSDMB expression groups. C Boxplot comparing TMB differences between the two groups. D Scatter plot of the correlation between TMB and GSDMB expression levels. E Kaplan-Meier survival curves for high and low TMB groups. F KM survival curves for four sample groups classified by combined TMB and GSDMB expression levels

Techniques Used: Expressing

Analysis of differences between the two groups and GSEA analysis results (330 OSCC tissues). A Volcano plot displaying DEGs. B Heatmap of DEGs illustrating expression levels across samples. C Circle plot combined with a network view of GO/KEGG pathway enrichment analysis. D Bar plot summarizing the results of GO/KEGG enrichment analysis. E - L Gene set enrichment analysis (GSEA) results for key KEGG pathways. Specific pathways include ECM-receptor interaction ( E ), focal adhesion ( F ), MAPK signaling ( G ), natural killer cell-mediated cytotoxicity ( H ), primary immunodeficiency ( I ), T-cell receptor signaling ( J ), TGF-beta signaling ( K ), and Toll-like receptor signaling ( L ). Key statistics (NES: Normalized Enrichment Score; p-value; FDR: False Discovery Rate) are provided in the plots

Figure Legend Snippet: Analysis of differences between the two groups and GSEA analysis results (330 OSCC tissues). A Volcano plot displaying DEGs. B Heatmap of DEGs illustrating expression levels across samples. C Circle plot combined with a network view of GO/KEGG pathway enrichment analysis. D Bar plot summarizing the results of GO/KEGG enrichment analysis. E - L Gene set enrichment analysis (GSEA) results for key KEGG pathways. Specific pathways include ECM-receptor interaction ( E ), focal adhesion ( F ), MAPK signaling ( G ), natural killer cell-mediated cytotoxicity ( H ), primary immunodeficiency ( I ), T-cell receptor signaling ( J ), TGF-beta signaling ( K ), and Toll-like receptor signaling ( L ). Key statistics (NES: Normalized Enrichment Score; p-value; FDR: False Discovery Rate) are provided in the plots

Techniques Used: Expressing

Basic analysis results of scRNA-seq data. A Violin plots of six OSCC samples' scRNA-seq data post-merging and quality control, indicating the number of nonzero-expressed genes per cell, total UMI counts, and mitochondrial gene percentage. B Two-dimensional distribution of six samples with batch effects. C Distribution of different samples after removing batch effects using the

Figure Legend Snippet: Basic analysis results of scRNA-seq data. A Violin plots of six OSCC samples' scRNA-seq data post-merging and quality control, indicating the number of nonzero-expressed genes per cell, total UMI counts, and mitochondrial gene percentage. B Two-dimensional distribution of six samples with batch effects. C Distribution of different samples after removing batch effects using the "Harmony" package in R. D Heatmap predicting cell cluster identities using the "singleR" software package. E Two-dimensional distribution of different cell types. F Expression of GSDMB in different cell types. G Distribution of six OSCC samples across different cell types

Techniques Used: Control, Software, Expressing

Classification of high and low expression cell clusters and GSDMB expression in stRNA-seq data. A All cells were divided into high and low expression clusters based on the median value of GSDMB. B Proportions of different cell types within high and low expression clusters. C Results of GSEA analysis for the two clusters. D Clustering results for four slices based on OSCC stRNA-seq data. E Cell type annotation results for four slices from OSCC stRNA-seq data. F Expression of GSDMB in different cell types

Figure Legend Snippet: Classification of high and low expression cell clusters and GSDMB expression in stRNA-seq data. A All cells were divided into high and low expression clusters based on the median value of GSDMB. B Proportions of different cell types within high and low expression clusters. C Results of GSEA analysis for the two clusters. D Clustering results for four slices based on OSCC stRNA-seq data. E Cell type annotation results for four slices from OSCC stRNA-seq data. F Expression of GSDMB in different cell types

Techniques Used: Expressing

GSDMB silencing attenuates the malignant properties and modulates 5-FU induced pyroptosis related responses in SCC25 cells. A IHC analysis of GSDMB expression in OSCC tissues and normal oral mucosa (n = 40). B – C Western blot analysis of GSDMB protein levels in HOK and OSCC cell lines and in SCC25 cells following siRNA transfection. D Cell viability assessed by the CCK-8 assay. E Representative images and quantification of colony formation. F Wound healing assay evaluating cell migration. G Transwell invasion assay. H Dose–response curves and corresponding IC50 values for 5-fluorouracil (5-FU). I Lactate dehydrogenase (LDH) release assay assessing 5-FU induced lytic cell death. J – K ELISA quantification of IL-1β and IL-18 levels in culture supernatants after 5-FU treatment. (* p < 0.05, ** p < 0.01, *** p < 0.001)

Figure Legend Snippet: GSDMB silencing attenuates the malignant properties and modulates 5-FU induced pyroptosis related responses in SCC25 cells. A IHC analysis of GSDMB expression in OSCC tissues and normal oral mucosa (n = 40). B – C Western blot analysis of GSDMB protein levels in HOK and OSCC cell lines and in SCC25 cells following siRNA transfection. D Cell viability assessed by the CCK-8 assay. E Representative images and quantification of colony formation. F Wound healing assay evaluating cell migration. G Transwell invasion assay. H Dose–response curves and corresponding IC50 values for 5-fluorouracil (5-FU). I Lactate dehydrogenase (LDH) release assay assessing 5-FU induced lytic cell death. J – K ELISA quantification of IL-1β and IL-18 levels in culture supernatants after 5-FU treatment. (* p < 0.05, ** p < 0.01, *** p < 0.001)

Techniques Used: Expressing, Western Blot, Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Lactate Dehydrogenase Assay, Enzyme-linked Immunosorbent Assay

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Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: Expression landscape of GSDMB across different groups (330 OSCC tissues, 32 normal tissues). A - C Differential expression of GSDMB among Grade categories, age groups, and N stages. D Boxplot showing the expression difference of GSDMB between OSCC cases and controls. E Receiver Operating Characteristic (ROC) curve for GSDMB. F Forest plot from univariate Cox regression analysis based on GSDMB expression levels and prognostic outcomes across various cancers. G Boxplot illustrating differences in GSDMB expression between control and disease groups across pan-cancer samples. “wilcox.test” is used to calculate the significance p-value (* p<0.05, ** p<0.01, *** p<0.001)

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Expressing, Quantitative Proteomics, Control

Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: Landscape of Tumor Mutational Burden (TMB) in high and low GSDMB expression groups (318 OSCC tissues). A - B Waterfall plots depicting mutations in high and low GSDMB expression groups. C Boxplot comparing TMB differences between the two groups. D Scatter plot of the correlation between TMB and GSDMB expression levels. E Kaplan-Meier survival curves for high and low TMB groups. F KM survival curves for four sample groups classified by combined TMB and GSDMB expression levels

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Expressing

Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: Analysis of differences between the two groups and GSEA analysis results (330 OSCC tissues). A Volcano plot displaying DEGs. B Heatmap of DEGs illustrating expression levels across samples. C Circle plot combined with a network view of GO/KEGG pathway enrichment analysis. D Bar plot summarizing the results of GO/KEGG enrichment analysis. E - L Gene set enrichment analysis (GSEA) results for key KEGG pathways. Specific pathways include ECM-receptor interaction ( E ), focal adhesion ( F ), MAPK signaling ( G ), natural killer cell-mediated cytotoxicity ( H ), primary immunodeficiency ( I ), T-cell receptor signaling ( J ), TGF-beta signaling ( K ), and Toll-like receptor signaling ( L ). Key statistics (NES: Normalized Enrichment Score; p-value; FDR: False Discovery Rate) are provided in the plots

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Expressing

Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: Basic analysis results of scRNA-seq data. A Violin plots of six OSCC samples' scRNA-seq data post-merging and quality control, indicating the number of nonzero-expressed genes per cell, total UMI counts, and mitochondrial gene percentage. B Two-dimensional distribution of six samples with batch effects. C Distribution of different samples after removing batch effects using the "Harmony" package in R. D Heatmap predicting cell cluster identities using the "singleR" software package. E Two-dimensional distribution of different cell types. F Expression of GSDMB in different cell types. G Distribution of six OSCC samples across different cell types

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Control, Software, Expressing

Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: Classification of high and low expression cell clusters and GSDMB expression in stRNA-seq data. A All cells were divided into high and low expression clusters based on the median value of GSDMB. B Proportions of different cell types within high and low expression clusters. C Results of GSEA analysis for the two clusters. D Clustering results for four slices based on OSCC stRNA-seq data. E Cell type annotation results for four slices from OSCC stRNA-seq data. F Expression of GSDMB in different cell types

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Expressing

Journal: BMC Oral Health

Article Title: Expression profile of GSDMB in oral squamous cell carcinoma and its impact on tumor immune microenvironment and prognosis

doi: 10.1186/s12903-026-07781-1

Figure Lengend Snippet: GSDMB silencing attenuates the malignant properties and modulates 5-FU induced pyroptosis related responses in SCC25 cells. A IHC analysis of GSDMB expression in OSCC tissues and normal oral mucosa (n = 40). B – C Western blot analysis of GSDMB protein levels in HOK and OSCC cell lines and in SCC25 cells following siRNA transfection. D Cell viability assessed by the CCK-8 assay. E Representative images and quantification of colony formation. F Wound healing assay evaluating cell migration. G Transwell invasion assay. H Dose–response curves and corresponding IC50 values for 5-fluorouracil (5-FU). I Lactate dehydrogenase (LDH) release assay assessing 5-FU induced lytic cell death. J – K ELISA quantification of IL-1β and IL-18 levels in culture supernatants after 5-FU treatment. (* p < 0.05, ** p < 0.01, *** p < 0.001)

Article Snippet: The human OSCC cell lines SCC4 and SCC25 were purchased from the American Type Culture Collection (ATCC, USA).

Techniques: Expressing, Western Blot, Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Lactate Dehydrogenase Assay, Enzyme-linked Immunosorbent Assay

CX3CL1 was upregulated in oral squamous cell carcinoma (OSCC) tissue and associated with clinical disease stages in human OSCC. (A) Correlation CX3CL1 gene expression with the normal and tumour cells using GEO microarray 3524 OSCC tissue samples. (B) CX3CL1 expression profiles in 497 OSCC tissue specimens were analysed obtained from the Cancer Genome Atlas (TCGA) database. (C,D) OSCC specimens were subjected to IHC staining. (E) Kaplan–Meier survival analysis of the associations between high or low plasma levels of CX3CL1 expression and overall survival of OSCC patients. * p < 0.05 compared with controls.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 was upregulated in oral squamous cell carcinoma (OSCC) tissue and associated with clinical disease stages in human OSCC. (A) Correlation CX3CL1 gene expression with the normal and tumour cells using GEO microarray 3524 OSCC tissue samples. (B) CX3CL1 expression profiles in 497 OSCC tissue specimens were analysed obtained from the Cancer Genome Atlas (TCGA) database. (C,D) OSCC specimens were subjected to IHC staining. (E) Kaplan–Meier survival analysis of the associations between high or low plasma levels of CX3CL1 expression and overall survival of OSCC patients. * p < 0.05 compared with controls.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Gene Expression, Microarray, Expressing, Immunohistochemistry, Clinical Proteomics

CX3CL1 upregulates human oral squamous cell carcinoma (OSCC) cell migration and invasion. (A‐C) OSCC cells were incubated with different concentrations of CX3CL1 for 24 h; then, cell migration was assessed using the (A) in vitro wound‐healing assay, (B,C) the Transwell assay. (D) Quantified result of cell migration with CX3CL1 neutralizing antibody. (E) Quantified result of cell invasion with CX3CL1 neutralizing antibody. Results are expressed as the mean ± SD of four independent experiments. * p < 0.05 as compared with controls.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 upregulates human oral squamous cell carcinoma (OSCC) cell migration and invasion. (A‐C) OSCC cells were incubated with different concentrations of CX3CL1 for 24 h; then, cell migration was assessed using the (A) in vitro wound‐healing assay, (B,C) the Transwell assay. (D) Quantified result of cell migration with CX3CL1 neutralizing antibody. (E) Quantified result of cell invasion with CX3CL1 neutralizing antibody. Results are expressed as the mean ± SD of four independent experiments. * p < 0.05 as compared with controls.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Migration, Incubation, In Vitro, Wound Healing Assay, Transwell Assay

CX3CL1 activates tumour cell migration via the ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A) ICAM‐1 expression in the normal and tumour cells obtained from the TCGA dataset analysis. (B) VCAM‐1 expression in the normal and tumour cells obtained from the TCGA dataset analysis. (C) Correlation analysis of CX3CL1 and ICAM‐1 expression using the TIMER2.0 database. (D) Correlation analysis of CX3CL1 and VCAM‐1 expression using the TIMER2.0 database. (E) Quantified result of ICAM‐1 gene expression with CX3CL1 recombinant protein (30 ng/mL) treatment. (F) Quantified result of VCAM‐1 gene expression with CX3CL1 recombinant protein (30 ng/mL) treatment. (G) Protein expression of ICAM‐1 with concentration‐depended CX3CL1 treatment. (H) Protein expression of VCAM‐1 with concentration‐depended CX3CL1 treatment. (I) Quantified result of cell migration with ICAM‐1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (J) Quantified result of cell migration with ICAM‐1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 activates tumour cell migration via the ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A) ICAM‐1 expression in the normal and tumour cells obtained from the TCGA dataset analysis. (B) VCAM‐1 expression in the normal and tumour cells obtained from the TCGA dataset analysis. (C) Correlation analysis of CX3CL1 and ICAM‐1 expression using the TIMER2.0 database. (D) Correlation analysis of CX3CL1 and VCAM‐1 expression using the TIMER2.0 database. (E) Quantified result of ICAM‐1 gene expression with CX3CL1 recombinant protein (30 ng/mL) treatment. (F) Quantified result of VCAM‐1 gene expression with CX3CL1 recombinant protein (30 ng/mL) treatment. (G) Protein expression of ICAM‐1 with concentration‐depended CX3CL1 treatment. (H) Protein expression of VCAM‐1 with concentration‐depended CX3CL1 treatment. (I) Quantified result of cell migration with ICAM‐1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (J) Quantified result of cell migration with ICAM‐1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Migration, Expressing, Gene Expression, Recombinant, Concentration Assay, Control

CX3CL1 upregulates cell motility and ICAM‐1 expression via its receptor CX3CR1. (A) Levels of CX3CR1 mRNA expression in normal tongue tissue and human oral squamous cell carcinoma (OSCC) tumour tissue were analysed using records from the GEO data set GSE13601. (B) Levels of CX3CR1 mRNA expression in different N stages of OSCC tumour tissue were analysed using records from the GEO data set GSE78060. (C) Quantified result of cell movement with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (D) Quantified result of cell migration with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Quantified resulting of ICAM‐1 expression with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (F) Quantified result of cell movement with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (G) Quantified result of cell migration with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (H) Quantified result of ICAM‐1 expression with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 upregulates cell motility and ICAM‐1 expression via its receptor CX3CR1. (A) Levels of CX3CR1 mRNA expression in normal tongue tissue and human oral squamous cell carcinoma (OSCC) tumour tissue were analysed using records from the GEO data set GSE13601. (B) Levels of CX3CR1 mRNA expression in different N stages of OSCC tumour tissue were analysed using records from the GEO data set GSE78060. (C) Quantified result of cell movement with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (D) Quantified result of cell migration with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Quantified resulting of ICAM‐1 expression with CX3CR1 neutralizing antibody and CX3CL1 recombinant protein (30 ng/mL) treatment. (F) Quantified result of cell movement with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (G) Quantified result of cell migration with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. (H) Quantified result of ICAM‐1 expression with CX3CR1 siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Expressing, Recombinant, Migration, Control

CX3CL1 triggers the phosphorylation of PLCβ/PKCα/c‐Src to signal the cell movement, migration and ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A‐C) Quantified result of cell movement, cell migration and ICAM‐1 expression with signalling inhibitors and CX3CL1 recombinant protein (30 ng/mL) treatment. (D‐E) Protein expression of phosphorylated PLCβ, PKCα and c‐Src with CX3CL1 recombinant protein (30 ng/mL) treatment in SCC4 cell and SAS cell. (F‐H) Quantified result of cell movement, cell migration and ICAM‐1 expression with PLCβ, PKCα or c‐Src siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 triggers the phosphorylation of PLCβ/PKCα/c‐Src to signal the cell movement, migration and ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A‐C) Quantified result of cell movement, cell migration and ICAM‐1 expression with signalling inhibitors and CX3CL1 recombinant protein (30 ng/mL) treatment. (D‐E) Protein expression of phosphorylated PLCβ, PKCα and c‐Src with CX3CL1 recombinant protein (30 ng/mL) treatment in SCC4 cell and SAS cell. (F‐H) Quantified result of cell movement, cell migration and ICAM‐1 expression with PLCβ, PKCα or c‐Src siRNA and CX3CL1 recombinant protein (30 ng/mL) treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Phospho-proteomics, Migration, Expressing, Recombinant, Control

CX3CL1 promotes the phosphorylation of c‐Jun to upregulate the cell motility and ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A) Quantified result of CX3CL1‐induced cell movement with c‐Jun inhibitors (B) Quantified result of CX3CL1‐induced cell migration with c‐Jun inhibitors (C) Quantified result of CX3CL1‐induced ICAM‐1 expression with c‐Jun inhibitors (D) Protein expression of phosphorylated c‐Jun with CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Quantified result of CX3CL1‐induced cell movement with c‐Jun siRNA treatment. (F) Quantified result of CX3CL1‐induced cell migration with c‐Jun siRNA treatment. (G) Quantified result of CX3CL1‐induced ICAM‐1 expression with c‐Jun siRNA treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 promotes the phosphorylation of c‐Jun to upregulate the cell motility and ICAM‐1 expression in human oral squamous cell carcinoma (OSCC) cells. (A) Quantified result of CX3CL1‐induced cell movement with c‐Jun inhibitors (B) Quantified result of CX3CL1‐induced cell migration with c‐Jun inhibitors (C) Quantified result of CX3CL1‐induced ICAM‐1 expression with c‐Jun inhibitors (D) Protein expression of phosphorylated c‐Jun with CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Quantified result of CX3CL1‐induced cell movement with c‐Jun siRNA treatment. (F) Quantified result of CX3CL1‐induced cell migration with c‐Jun siRNA treatment. (G) Quantified result of CX3CL1‐induced ICAM‐1 expression with c‐Jun siRNA treatment. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Phospho-proteomics, Expressing, Migration, Recombinant, Control

CX3CL1 promotes the translocation of c‐Jun and promoter binding of AP‐1 formation in human oral squamous cell carcinoma (OSCC) cells. (A) Immunofluorescent staining showed that c‐Jun translocated into the nucleus after cell were treated with CX3CL1; nuclear translocation was prevented when the cells were pre‐treated with CX3CR1 mAb, U73122, GF109203 or PP2. (B) Quantified analysis of c‐Jun activation with CX3CL1 using Western blot. (C) CX3CL1 treatment upregulated AP‐1 luciferase activity. (D) Quantified analysis of AP‐1 luciferase activity with specific inhibitors and CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Chromatin immunoprecipitation analysis of c‐Jun and AP‐1 promoter binding site with neutralizing antibody and specific inhibitors. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CX3CL1 induces cell migration and invasion through ICAM ‐1 expression in oral squamous cell carcinoma cells

doi: 10.1111/jcmm.17750

Figure Lengend Snippet: CX3CL1 promotes the translocation of c‐Jun and promoter binding of AP‐1 formation in human oral squamous cell carcinoma (OSCC) cells. (A) Immunofluorescent staining showed that c‐Jun translocated into the nucleus after cell were treated with CX3CL1; nuclear translocation was prevented when the cells were pre‐treated with CX3CR1 mAb, U73122, GF109203 or PP2. (B) Quantified analysis of c‐Jun activation with CX3CL1 using Western blot. (C) CX3CL1 treatment upregulated AP‐1 luciferase activity. (D) Quantified analysis of AP‐1 luciferase activity with specific inhibitors and CX3CL1 recombinant protein (30 ng/mL) treatment. (E) Chromatin immunoprecipitation analysis of c‐Jun and AP‐1 promoter binding site with neutralizing antibody and specific inhibitors. Results are expressed as the mean ± SD of four independent experiments. *, p < 0.05 and #, p < 0.05 as compared to control and CX3CL1 treatment.

Article Snippet: Three human OSCC cell lines (SCC4, SCC25 and SAS cells) were acquired from the Bioresource Collection and Research Center (BCRC).

Techniques: Translocation Assay, Binding Assay, Staining, Activation Assay, Western Blot, Luciferase, Activity Assay, Recombinant, Chromatin Immunoprecipitation, Control

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