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JCRB Cell Bank the human oscc cell lines sas, ca9-22, and hsc-3
The Human Oscc Cell Lines Sas, Ca9 22, And Hsc 3, supplied by JCRB Cell Bank, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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the human oscc cell lines sas, ca9-22, and hsc-3 - by Bioz Stars, 2026-10

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Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis
Article Snippet: human keratinocyte cell line HaCaT was purchased from the Kunming Cell Bank of the Chinese Academy of Sciences (Kunming, China). .. The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan). .. The CAL-27 cell line was obtained from the National Infrastructure of Cell Line Resources (NICR, Wuhan, China), All cells were cultu

Microarray:

Immunohistochemistry:

Software:

Quantitative RT-PCR:

Western Blot:

Migration:

Over Expression:

Transfection:

Plasmid Preparation:

Wound Healing Assay:

Immunofluorescence:

Staining:

Inhibition:

Clone Assay:

Luciferase:

Construct:

Activity Assay:

Transwell Migration Assay:

Transwell Invasion Assay:

In Vivo:

Injection:

Stable Transfection:

Image Search Results

The expression of SMARCA4 is upregulated in OSCC. ( A , B ) A tissue microarray of human OSCC and normal tissues was analyzed by IHC staining using the Image ProPlus software (version1 1.48). ( C ) Comparison of SMARCA4 mRNA expression levels in OSCC cell lines (SAS, CAL-27) with that in HaCat cells by qRT-PCR analysis. Data are expressed as the mean ± SEM from triplicates experiments. * p < 0.05, ** p < 0.01. ( D ) Comparison of SMARCA4 protein expression levels in OSCC cell lines (SAS, CAL-27) with that in HaCat cells by western blot analysis.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: The expression of SMARCA4 is upregulated in OSCC. ( A , B ) A tissue microarray of human OSCC and normal tissues was analyzed by IHC staining using the Image ProPlus software (version1 1.48). ( C ) Comparison of SMARCA4 mRNA expression levels in OSCC cell lines (SAS, CAL-27) with that in HaCat cells by qRT-PCR analysis. Data are expressed as the mean ± SEM from triplicates experiments. * p < 0.05, ** p < 0.01. ( D ) Comparison of SMARCA4 protein expression levels in OSCC cell lines (SAS, CAL-27) with that in HaCat cells by western blot analysis.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Expressing, Microarray, Immunohistochemistry, Software, Quantitative RT-PCR, Western Blot

SMARCA4 promotes OSCC cell migration and invasion. ( A , B ) The effect of SMARCA4 overexpression on OSCC cell migration. SAS or CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was assessed by the wound healing assay. Scale bar: 100 µm ( A ). Quantitative analysis was performed using the Image J version 1.48 software ( B ). ( C , D ) The effect of SMARCA4 overexpression on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration and invasion were assessed by Transwell migration and invasion assays. Scale bar: 200 µm ( C ). Quantitative analysis was performed using the Image J software ( D ). ( E , F ) Representative images of E-cadherin and vimentin expression in SAS cells detected by immunofluorescence staining after SAS cells were transfected with SMARCA4 overexpression plasmid or control vector for 48 h (Scale bar: 20 µm, green represents E-cadherin, red represents vimentin, and nucleus is shown in blue by DAPI staining). ( G ) The effect of SMARCA4 overexpression on OSCC cell E-cadherin and vimentin protein expression levels. SAS and CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for 48 h, and the E-cadherin or vimentin protein expression levels were measured by Western blot analysis. ( H ) Quantitative analysis was performed using the Image J software. Data are expressed as the mean ± SEM from triplicate experiments. ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs control vector group.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: SMARCA4 promotes OSCC cell migration and invasion. ( A , B ) The effect of SMARCA4 overexpression on OSCC cell migration. SAS or CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was assessed by the wound healing assay. Scale bar: 100 µm ( A ). Quantitative analysis was performed using the Image J version 1.48 software ( B ). ( C , D ) The effect of SMARCA4 overexpression on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration and invasion were assessed by Transwell migration and invasion assays. Scale bar: 200 µm ( C ). Quantitative analysis was performed using the Image J software ( D ). ( E , F ) Representative images of E-cadherin and vimentin expression in SAS cells detected by immunofluorescence staining after SAS cells were transfected with SMARCA4 overexpression plasmid or control vector for 48 h (Scale bar: 20 µm, green represents E-cadherin, red represents vimentin, and nucleus is shown in blue by DAPI staining). ( G ) The effect of SMARCA4 overexpression on OSCC cell E-cadherin and vimentin protein expression levels. SAS and CAL-27 cells were transfected with SMARCA4 overexpression plasmid or control vector for 48 h, and the E-cadherin or vimentin protein expression levels were measured by Western blot analysis. ( H ) Quantitative analysis was performed using the Image J software. Data are expressed as the mean ± SEM from triplicate experiments. ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs control vector group.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration, Over Expression, Transfection, Plasmid Preparation, Wound Healing Assay, Software, Expressing, Immunofluorescence, Staining, Western Blot

Knockdown of SMARCA4 inhibits OSCC cell migration and invasion. ( A – D ) The effect of SMARCA4 inhibition on OSCC cell migration. SAS or CAL-27 cells were transfected with sh-SMARCA4 or sh-NC for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was assessed by the wound healing assay. Scale bar: 100 µm ( A , B ). Quantitative analysis was performed using the Image J software ( C , D ). ( E – H ) The effect of SMARCA4 inhibition on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with sh-SMARCA4 or sh-NC for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration ( E ) and invasion ( F ) were assessed by Transwell migration and invasion assays. Scale bar: 200 µm. Quantitative analysis was performed using the Image J software ( G , H ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p <0.0001 vs shNC group.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: Knockdown of SMARCA4 inhibits OSCC cell migration and invasion. ( A – D ) The effect of SMARCA4 inhibition on OSCC cell migration. SAS or CAL-27 cells were transfected with sh-SMARCA4 or sh-NC for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was assessed by the wound healing assay. Scale bar: 100 µm ( A , B ). Quantitative analysis was performed using the Image J software ( C , D ). ( E – H ) The effect of SMARCA4 inhibition on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with sh-SMARCA4 or sh-NC for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration ( E ) and invasion ( F ) were assessed by Transwell migration and invasion assays. Scale bar: 200 µm. Quantitative analysis was performed using the Image J software ( G , H ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p <0.0001 vs shNC group.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration, Inhibition, Transfection, Wound Healing Assay, Software

SMARCA4 is a target gene of miR-199a-5p in OSCC cells. ( A ) The alignment between miR-199a-5p and WT or MUT SMARCA4 3′UTR region. ( B , C ) SMARCA4 3′UTR containing a miR-199a-5p WT or a MUT target site was cloned into the luciferase reporter vector. These constructs were co-transfected with miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor, or inhibitor NC into 293T cells. Luciferase activity was measured after 48 h. ( D , E ) The transfection efficiency of miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor or inhibitor NC in OSCC cells. SAS or CAL-27 were transfected with miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor, or inhibitor NC for 48 h. The expression level of miR-199a-5p in OSCC cells was measured by qRT-PCR. ( F , G ) The effect of miR-199a-5p on SMARCA4 mRNA expression level in OSCC cells. SAS or CAL-27 cells were transfected with miR-199a-5p mimics ( F ) or miR-199a-5p inhibitors for 48 h ( G ). The mRNA expression level of SMARCA4 in OSCC cells was measured by qRT-PCR. ( H , I ) The effect of miR-199a-5p on SMARCA4 protein expression level in OSCC cells. SAS or CAL-27 cells were transfected with miR-199a-5p mimics ( H ) or miR-199a-5p inhibitors for 48 h ( I ). SMARCA4 protein level was measured by Western blot analysis. GAPDH was used as a loading control. Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, **** p < 0.001, comparison with the corresponding control.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: SMARCA4 is a target gene of miR-199a-5p in OSCC cells. ( A ) The alignment between miR-199a-5p and WT or MUT SMARCA4 3′UTR region. ( B , C ) SMARCA4 3′UTR containing a miR-199a-5p WT or a MUT target site was cloned into the luciferase reporter vector. These constructs were co-transfected with miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor, or inhibitor NC into 293T cells. Luciferase activity was measured after 48 h. ( D , E ) The transfection efficiency of miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor or inhibitor NC in OSCC cells. SAS or CAL-27 were transfected with miR-199a-5p mimics, mimics NC, miR-199a-5p inhibitor, or inhibitor NC for 48 h. The expression level of miR-199a-5p in OSCC cells was measured by qRT-PCR. ( F , G ) The effect of miR-199a-5p on SMARCA4 mRNA expression level in OSCC cells. SAS or CAL-27 cells were transfected with miR-199a-5p mimics ( F ) or miR-199a-5p inhibitors for 48 h ( G ). The mRNA expression level of SMARCA4 in OSCC cells was measured by qRT-PCR. ( H , I ) The effect of miR-199a-5p on SMARCA4 protein expression level in OSCC cells. SAS or CAL-27 cells were transfected with miR-199a-5p mimics ( H ) or miR-199a-5p inhibitors for 48 h ( I ). SMARCA4 protein level was measured by Western blot analysis. GAPDH was used as a loading control. Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, **** p < 0.001, comparison with the corresponding control.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Clone Assay, Luciferase, Plasmid Preparation, Construct, Transfection, Activity Assay, Expressing, Quantitative RT-PCR, Western Blot

Effect of miR-199a-5p on OSCC cells EMT and migration. ( A ) Comparison of miR-199a-5p mRNA levels in SAS, CAL-27, and HaCaT. The miR-199a-5p mRNA level was detected by qRT-PCR. ( B ) The effect of miR-199a-5p mimics on OSCC cell E-cadherin and vimentin protein expression levels. SAS and CAL-27 cells were transfected with miR-199a-5p mimics 48h, and the E-cadherin or vimentin protein expression levels were measured by Western blot analysis. ( C ) The protein bands were analyzed by Image J. ( D – G ) The effect of miR-199a-5p mimics or miR-199a-5p inhibitor on OSCC cell migration. SAS cells or CAL-27 cells were transfected with miR-199a-5p mimics or miR-199a-5p inhibitor for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was measured by the wound healing assay. Scale bar: 100 µm ( D , F ). Quantitative analysis was performed using the Image J software ( E , G ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: Effect of miR-199a-5p on OSCC cells EMT and migration. ( A ) Comparison of miR-199a-5p mRNA levels in SAS, CAL-27, and HaCaT. The miR-199a-5p mRNA level was detected by qRT-PCR. ( B ) The effect of miR-199a-5p mimics on OSCC cell E-cadherin and vimentin protein expression levels. SAS and CAL-27 cells were transfected with miR-199a-5p mimics 48h, and the E-cadherin or vimentin protein expression levels were measured by Western blot analysis. ( C ) The protein bands were analyzed by Image J. ( D – G ) The effect of miR-199a-5p mimics or miR-199a-5p inhibitor on OSCC cell migration. SAS cells or CAL-27 cells were transfected with miR-199a-5p mimics or miR-199a-5p inhibitor for the indicated times (6 h for SAS, 30 h for CAL-27), and cell migration was measured by the wound healing assay. Scale bar: 100 µm ( D , F ). Quantitative analysis was performed using the Image J software ( E , G ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration, Quantitative RT-PCR, Expressing, Transfection, Western Blot, Wound Healing Assay, Software

MiR-199a-5p inhibits OSCC cell migration and invasion. The effect of miR-199a-5p mimics or miR-199a-5p inhibitors on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with miR-199a-5p mimics or miR-199a-5p inhibitors for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration ( A ) and invasion ( C ) were assessed by Transwell migration and invasion assays. Scale bar: 200 µm. Quantitative analysis was performed using the Image J software ( B , D ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: MiR-199a-5p inhibits OSCC cell migration and invasion. The effect of miR-199a-5p mimics or miR-199a-5p inhibitors on OSCC cell migration and invasion. SAS or CAL-27 cells were transfected with miR-199a-5p mimics or miR-199a-5p inhibitors for the indicated times (24 h for SAS, 48 h for CAL-27). Cell migration ( A ) and invasion ( C ) were assessed by Transwell migration and invasion assays. Scale bar: 200 µm. Quantitative analysis was performed using the Image J software ( B , D ). Data are expressed as the mean ± SEM from triplicate experiments. * p < 0.05, ** p < 0.01.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration, Transfection, Software

miR-199a-5p inhibits OSCC cell migration and invasion through the downregulation of SMARCA4. ( A – D ) The effect of SMARCA4 overexpression on miR-199a-5p mimics-induced OSCC cell migration and invasion inhibition. SAS cells were transfected with miR-199a-5p mimics, or miR-199a-5p mimics and SMARCA4 overexpression plasmid. Cell migration was measured by both the wound healing assay ( A ) and Transwell migration assay ( C ), and cell invasion was measured by the Transwell invasion assay ( C ). Quantitative analysis was performed by the Image J software ( B , D ). ( E – H ) The effect of SMARCA4 inhibition on miR-199a-5p inhibitor-induced OSCC cell migration and invasion. SAS cells were transfected with miR-199a-5p inhibitor, or miR-199a-5p inhibitor and sh-SMARCA4. Cell migration was measured by both the wound healing assay ( E ) and Transwell migration assay ( G ), and cell invasion was measured by the Transwell invasion assay ( G ). Quantitative analysis was performed by the Image J software ( F , H ). The scale bar is shown in lower-right corner. Data are expressed as the mean ± SEM from triplicate experiments. ** p < 0.01, *** p < 0.001, **** p < 0.0001, comparison with the corresponding controls.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: miR-199a-5p inhibits OSCC cell migration and invasion through the downregulation of SMARCA4. ( A – D ) The effect of SMARCA4 overexpression on miR-199a-5p mimics-induced OSCC cell migration and invasion inhibition. SAS cells were transfected with miR-199a-5p mimics, or miR-199a-5p mimics and SMARCA4 overexpression plasmid. Cell migration was measured by both the wound healing assay ( A ) and Transwell migration assay ( C ), and cell invasion was measured by the Transwell invasion assay ( C ). Quantitative analysis was performed by the Image J software ( B , D ). ( E – H ) The effect of SMARCA4 inhibition on miR-199a-5p inhibitor-induced OSCC cell migration and invasion. SAS cells were transfected with miR-199a-5p inhibitor, or miR-199a-5p inhibitor and sh-SMARCA4. Cell migration was measured by both the wound healing assay ( E ) and Transwell migration assay ( G ), and cell invasion was measured by the Transwell invasion assay ( G ). Quantitative analysis was performed by the Image J software ( F , H ). The scale bar is shown in lower-right corner. Data are expressed as the mean ± SEM from triplicate experiments. ** p < 0.01, *** p < 0.001, **** p < 0.0001, comparison with the corresponding controls.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration, Over Expression, Inhibition, Transfection, Plasmid Preparation, Wound Healing Assay, Transwell Migration Assay, Transwell Invasion Assay, Software

Knockdown of SMARCA4 suppresses OSCC tumorigenesis associated with upregulated miR199-a-5p in vivo. ( A ) Xenograft nude mice were injected with SAS cells stably transfected with sh-SMARCA4 or sh-NC. After 2 weeks, the mice were sacrificed, and the tumors were collected. The tumor size was measured using a caliper. ( n = 5, each group). ( B ) Comparison of tumor growth rate between the sh-SMARCA4 group and sh-NC group. ( C ) Comparison of tumor weight between the sh-SMARCA4 group and sh-NC group. ( D ) Representative IHC staining images of SMARCA4, E-cadherin, and vimentin protein in tumor tissues from the sh-SMARCA4group or sh-NC group (scare bars: 10 × : 100 µm, 40 × : 20 µm). ( E ) Comparison of SMARCA4 or miR199-a-5p mRNA expression levels in tumor tissues from the sh-SMARCA4 group and sh-NC group. * p < 0.05, *** p < 0.001, **** p < 0.0001, comparison with the sh-NC group.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: Knockdown of SMARCA4 suppresses OSCC tumorigenesis associated with upregulated miR199-a-5p in vivo. ( A ) Xenograft nude mice were injected with SAS cells stably transfected with sh-SMARCA4 or sh-NC. After 2 weeks, the mice were sacrificed, and the tumors were collected. The tumor size was measured using a caliper. ( n = 5, each group). ( B ) Comparison of tumor growth rate between the sh-SMARCA4 group and sh-NC group. ( C ) Comparison of tumor weight between the sh-SMARCA4 group and sh-NC group. ( D ) Representative IHC staining images of SMARCA4, E-cadherin, and vimentin protein in tumor tissues from the sh-SMARCA4group or sh-NC group (scare bars: 10 × : 100 µm, 40 × : 20 µm). ( E ) Comparison of SMARCA4 or miR199-a-5p mRNA expression levels in tumor tissues from the sh-SMARCA4 group and sh-NC group. * p < 0.05, *** p < 0.001, **** p < 0.0001, comparison with the sh-NC group.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: In Vivo, Injection, Stable Transfection, Transfection, Immunohistochemistry, Expressing

The proposed model for SMARCA4-promoted metastasis in OSCC. The miR-199a-5p -SMARCA4 axis regulates OSCC cell migration and invasion through EMT and plays a critical role in OSCC metastasis.

Journal: International Journal of Molecular Sciences

Article Title: MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis

doi: 10.3390/ijms24054756

Figure Lengend Snippet: The proposed model for SMARCA4-promoted metastasis in OSCC. The miR-199a-5p -SMARCA4 axis regulates OSCC cell migration and invasion through EMT and plays a critical role in OSCC metastasis.

Article Snippet: The human OSCC cell line SAS was purchased from Japanese Collection of Research Bioresources (JCRB) cell bank (Tokyo, Japan).

Techniques: Migration

Sensitivity of chemotherapeutic agents to CYLD-knockdown OSCC cells. Human OSCC cell line (SAS) cells were transfected with control siRNA (siN) or CYLD-specific siRNA (siCYLD) and then treated with cisplatin ( A ), 5-FU ( B ), carboplatin ( C ), docetaxel ( D ), and paclitaxel ( E ). The cell survival rates of SAS cells were assessed 72 h after treatment. Values are means ± S.D. of quadruple samples. **p < 0.01 vs siN group in Tukey–Kramer method

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Sensitivity of chemotherapeutic agents to CYLD-knockdown OSCC cells. Human OSCC cell line (SAS) cells were transfected with control siRNA (siN) or CYLD-specific siRNA (siCYLD) and then treated with cisplatin ( A ), 5-FU ( B ), carboplatin ( C ), docetaxel ( D ), and paclitaxel ( E ). The cell survival rates of SAS cells were assessed 72 h after treatment. Values are means ± S.D. of quadruple samples. **p < 0.01 vs siN group in Tukey–Kramer method

Article Snippet: Human OSCC cell line (SAS) cells were transfected with control siRNA (siN) or CYLD-specific siRNA (siCYLD) and then treated with cisplatin ( A ), 5-FU ( B ), carboplatin ( C ), docetaxel ( D ), and paclitaxel ( E ).

Techniques: Knockdown, Transfection, Control

Effect of CYLD down-regulation on intracellular signaling pathways in OSCC cells. A Comprehensive changes in protein expression by CYLD knockdown were assessed by proteome analysis. B KEGG database analysis of cell signaling pathways activated by CYLD knockdown. C Phosphorylation of Akt and ERK was assessed by immunoblotting. Cells were transfected with the indicated siRNAs and then incubated for 72 h before harvesting. Cell lysate was immunoblotted with antibodies against the indicated proteins. D Cells were treated with LY294002 (Akt Inhibitor, 20 µM), PD98059 (ERK Inhibitor, 20 µM), combination, and cisplatin (8 µg/mL). Cells survival rate are assessed after 72 h. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Effect of CYLD down-regulation on intracellular signaling pathways in OSCC cells. A Comprehensive changes in protein expression by CYLD knockdown were assessed by proteome analysis. B KEGG database analysis of cell signaling pathways activated by CYLD knockdown. C Phosphorylation of Akt and ERK was assessed by immunoblotting. Cells were transfected with the indicated siRNAs and then incubated for 72 h before harvesting. Cell lysate was immunoblotted with antibodies against the indicated proteins. D Cells were treated with LY294002 (Akt Inhibitor, 20 µM), PD98059 (ERK Inhibitor, 20 µM), combination, and cisplatin (8 µg/mL). Cells survival rate are assessed after 72 h. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method

Techniques: Protein-Protein interactions, Expressing, Knockdown, Phospho-proteomics, Western Blot, Transfection, Incubation

Involvement of EGFR in cell viability of CYLD-knockdown OSCC cells. A EGFR phosphorylation was assessed by immunoblotting in OSCC cells. Cells were transfected with siRNA and then incubated for 72 h before harvesting. Cell lysate was immunoblotted with antibodies against the indicated proteins. B Cells were treated with gefitinib (10 µM) and cisplatin (8 µg/mL), and cells survival rate was assessed after 72 h. Relative cell survival rate of siCYLD cells compared to that of siN cells after treatment with each anticancer drug was shown. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method. C (left panels) Representative images of cells treated with 10 µM gefitinib for 72 h. Scale bars show 100 µm. (right panel). Cell survival rates of OSCC cells were evaluated 72 h after treatment with various concentrations of gefitinib. Values are means ± S.D. of triplicate samples. **p < 0.01 vs siN group in Tukey–Kramer method. D Cells were treated with gefitinib (10 µM) and the cell survival rates were evaluated 24–72 h after treatment. Values are means ± S.D. of triplicate samples. * p < 0.05, ** p < 0.01 vs siN group in Tukey–Kramer method. (E) The gefitinib (10 µM)-induced apoptosis was assessed by Annexin-V/7-AAD staining using flow cytometry. Values are means ± S.D. of triplicate samples. n.s.: not significant, **p < 0.01 vs siN group in Tukey–Kramer method. F Phosphorylation of Akt and ERK were assessed by immunoblotting in OSCC cells treated with 10 µM gefitinib

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Involvement of EGFR in cell viability of CYLD-knockdown OSCC cells. A EGFR phosphorylation was assessed by immunoblotting in OSCC cells. Cells were transfected with siRNA and then incubated for 72 h before harvesting. Cell lysate was immunoblotted with antibodies against the indicated proteins. B Cells were treated with gefitinib (10 µM) and cisplatin (8 µg/mL), and cells survival rate was assessed after 72 h. Relative cell survival rate of siCYLD cells compared to that of siN cells after treatment with each anticancer drug was shown. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method. C (left panels) Representative images of cells treated with 10 µM gefitinib for 72 h. Scale bars show 100 µm. (right panel). Cell survival rates of OSCC cells were evaluated 72 h after treatment with various concentrations of gefitinib. Values are means ± S.D. of triplicate samples. **p < 0.01 vs siN group in Tukey–Kramer method. D Cells were treated with gefitinib (10 µM) and the cell survival rates were evaluated 24–72 h after treatment. Values are means ± S.D. of triplicate samples. * p < 0.05, ** p < 0.01 vs siN group in Tukey–Kramer method. (E) The gefitinib (10 µM)-induced apoptosis was assessed by Annexin-V/7-AAD staining using flow cytometry. Values are means ± S.D. of triplicate samples. n.s.: not significant, **p < 0.01 vs siN group in Tukey–Kramer method. F Phosphorylation of Akt and ERK were assessed by immunoblotting in OSCC cells treated with 10 µM gefitinib

Techniques: Knockdown, Phospho-proteomics, Western Blot, Transfection, Incubation, Staining, Flow Cytometry

Effect of EGFR targeted inhibitors on cell viability of CYLD-knockdown OSCC cells. Cells were treated with erlotinib ( A ), afatinib ( B ), osimertinib ( C ) and cetuximab ( D ), and the cell survival rates were assessed 72 h after treatment. Values Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 vs siN group in Tukey–Kramer method

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Effect of EGFR targeted inhibitors on cell viability of CYLD-knockdown OSCC cells. Cells were treated with erlotinib ( A ), afatinib ( B ), osimertinib ( C ) and cetuximab ( D ), and the cell survival rates were assessed 72 h after treatment. Values Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 vs siN group in Tukey–Kramer method

Techniques: Knockdown

Effect of EGFR targeted inhibitors on EMT-like changes in CYLD-knockdown OSCC cells. (A, E) SAS cells were treated with 5 μM gefitinib ( A ) and 10 µg/mL cetuximab ( E ), and Smad3 phosphorylation were assessed by immunoblotting. ( B , F ) Cell migration in SAS cells treated with 5 μM gefitinib ( B ) and 10 µg/mL cetuximab ( F ) was assessed by wound healing assay. ( C , G ) Cells were transfected with siRNA and then incubated for 48 h before being reseeded onto transwell insert. Cells were treated with 0.15 μM gefitinib ( C ) and 10 µg/mL cetuximab ( G ) for 24 h, and migrating cells were stained by crystal violet and then measured. D , H CYLD knockdown cells were treated with 5 μM gefitinib ( D ) and 10 µg/mL cetuximab ( H ) for 24 h, and Fibronectin mRNA expression was assessed by RT-qPCR. Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Effect of EGFR targeted inhibitors on EMT-like changes in CYLD-knockdown OSCC cells. (A, E) SAS cells were treated with 5 μM gefitinib ( A ) and 10 µg/mL cetuximab ( E ), and Smad3 phosphorylation were assessed by immunoblotting. ( B , F ) Cell migration in SAS cells treated with 5 μM gefitinib ( B ) and 10 µg/mL cetuximab ( F ) was assessed by wound healing assay. ( C , G ) Cells were transfected with siRNA and then incubated for 48 h before being reseeded onto transwell insert. Cells were treated with 0.15 μM gefitinib ( C ) and 10 µg/mL cetuximab ( G ) for 24 h, and migrating cells were stained by crystal violet and then measured. D , H CYLD knockdown cells were treated with 5 μM gefitinib ( D ) and 10 µg/mL cetuximab ( H ) for 24 h, and Fibronectin mRNA expression was assessed by RT-qPCR. Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method

Techniques: Knockdown, Phospho-proteomics, Western Blot, Migration, Wound Healing Assay, Transfection, Incubation, Staining, Expressing, Quantitative RT-PCR

Therapeutic effect of gefitinib and usefulness of CYLD as a novel biomarker in xenograft models. A , B SAS cells were injected subcutaneously into SCID mice (n = 6). After 7 days from cells injection, the tumor-inoculated CDX models were injected intraperitoneally with 2.5 mg gefitinib or DMSO, and tumor volume were measured at 14 days ( A ) in a time-dependent manner ( B ). Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey Kramer test. C Kaplan–Meier plot of overall survival of CDX models. **p < 0.01 siCYLD control group vs siCYLD gefitinib group in log-rank test. D PDX-derived cells (PDX st.1 & PDX st.2) were treated with gefitinib, and the cell survival rates were assessed 48 h after treatment. Values Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method. E Immunohistochemical analysis for CYLD expression in tumor tissues from PDX models (PDX st.1 & PDX st.2). CYLD positive rates were be calculated by ImageJ. Boxplots represented the first, second, and third quartiles, and whiskers extended to maximum value and minimum value except for outliers. Values Scale bar shows 40 µm. **p < 0.01 in Mann–Whitney U test. F Schematic model illustrating novel therapeutic strategies for CYLD-negative OSCC patients with poor prognosis

Journal: Cancer Cell International

Article Title: Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance

doi: 10.1186/s12935-022-02781-x

Figure Lengend Snippet: Therapeutic effect of gefitinib and usefulness of CYLD as a novel biomarker in xenograft models. A , B SAS cells were injected subcutaneously into SCID mice (n = 6). After 7 days from cells injection, the tumor-inoculated CDX models were injected intraperitoneally with 2.5 mg gefitinib or DMSO, and tumor volume were measured at 14 days ( A ) in a time-dependent manner ( B ). Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey Kramer test. C Kaplan–Meier plot of overall survival of CDX models. **p < 0.01 siCYLD control group vs siCYLD gefitinib group in log-rank test. D PDX-derived cells (PDX st.1 & PDX st.2) were treated with gefitinib, and the cell survival rates were assessed 48 h after treatment. Values Scale bar shows 200 µm. Values are means ± S.D. of triplicate samples. **p < 0.01 in Tukey–Kramer method. E Immunohistochemical analysis for CYLD expression in tumor tissues from PDX models (PDX st.1 & PDX st.2). CYLD positive rates were be calculated by ImageJ. Boxplots represented the first, second, and third quartiles, and whiskers extended to maximum value and minimum value except for outliers. Values Scale bar shows 40 µm. **p < 0.01 in Mann–Whitney U test. F Schematic model illustrating novel therapeutic strategies for CYLD-negative OSCC patients with poor prognosis

Techniques: Biomarker Discovery, Injection, Control, Derivative Assay, Immunohistochemical staining, Expressing, MANN-WHITNEY

Review

the human oscc cell lines sas, ca9-22, and hsc-3 (JCRB Cell Bank)

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Migration:

Over Expression:

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Wound Healing Assay:

Immunofluorescence:

Staining:

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