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scc15 cells  (ATCC)


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    Structured Review

    ATCC scc15 cells
    METTL5 is elevated in HNSCC and is associated with poor prognosis of HNSCC. (A) Comparison of mRNA levels of METTL5 in HNSCC with normal tissues in TCGA-HNSCC dataset. (B) Overall survival of patients between METTL5-high (n=259) and METTL5-low (n=259) groups. (C) METTL5 expression level in normal and HNSCC tissues with different stages of lymph node metastasis. (D) METTL5 expression level in normal tissues and different stages of HNSCC tissues. (E) METTL5 expression level in normal HNSCC tissues and different grades of HNSCC tissues. (F) METTL5 protein level in OSCC(HSC3, <t>SCC15)</t> and HOK cell lines. (G) Representative bands of METTL5 protein expression levels in human OSCC and paired normal tissues measured by western blotting. (H) Semi-quantification of METTL5 protein expression levels in human OSCC and paired normal tissues. *P<0.05, **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; HNSCC, head and neck squamous cell carcinoma; TCGA, The Cancer Genome Atlas; OSCC, oral squamous cell carcinoma; HOK, human normal oral epithelial keratinocyte; HR, hazard ratio; TPM, transcripts per million; N, normal; T, tumor.
    Scc15 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 707 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/scc15 cells/product/ATCC
    Average 96 stars, based on 707 article reviews
    scc15 cells - by Bioz Stars, 2026-04
    96/100 stars

    Images

    1) Product Images from "METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation"

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    Journal: Oncology Letters

    doi: 10.3892/ol.2026.15490

    METTL5 is elevated in HNSCC and is associated with poor prognosis of HNSCC. (A) Comparison of mRNA levels of METTL5 in HNSCC with normal tissues in TCGA-HNSCC dataset. (B) Overall survival of patients between METTL5-high (n=259) and METTL5-low (n=259) groups. (C) METTL5 expression level in normal and HNSCC tissues with different stages of lymph node metastasis. (D) METTL5 expression level in normal tissues and different stages of HNSCC tissues. (E) METTL5 expression level in normal HNSCC tissues and different grades of HNSCC tissues. (F) METTL5 protein level in OSCC(HSC3, SCC15) and HOK cell lines. (G) Representative bands of METTL5 protein expression levels in human OSCC and paired normal tissues measured by western blotting. (H) Semi-quantification of METTL5 protein expression levels in human OSCC and paired normal tissues. *P<0.05, **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; HNSCC, head and neck squamous cell carcinoma; TCGA, The Cancer Genome Atlas; OSCC, oral squamous cell carcinoma; HOK, human normal oral epithelial keratinocyte; HR, hazard ratio; TPM, transcripts per million; N, normal; T, tumor.
    Figure Legend Snippet: METTL5 is elevated in HNSCC and is associated with poor prognosis of HNSCC. (A) Comparison of mRNA levels of METTL5 in HNSCC with normal tissues in TCGA-HNSCC dataset. (B) Overall survival of patients between METTL5-high (n=259) and METTL5-low (n=259) groups. (C) METTL5 expression level in normal and HNSCC tissues with different stages of lymph node metastasis. (D) METTL5 expression level in normal tissues and different stages of HNSCC tissues. (E) METTL5 expression level in normal HNSCC tissues and different grades of HNSCC tissues. (F) METTL5 protein level in OSCC(HSC3, SCC15) and HOK cell lines. (G) Representative bands of METTL5 protein expression levels in human OSCC and paired normal tissues measured by western blotting. (H) Semi-quantification of METTL5 protein expression levels in human OSCC and paired normal tissues. *P<0.05, **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; HNSCC, head and neck squamous cell carcinoma; TCGA, The Cancer Genome Atlas; OSCC, oral squamous cell carcinoma; HOK, human normal oral epithelial keratinocyte; HR, hazard ratio; TPM, transcripts per million; N, normal; T, tumor.

    Techniques Used: Comparison, Expressing, Western Blot

    Knockout of METTL5 inhibits the progression of OSCC in vitro . (A) Validation of METTL5 stable knockout in SCC15 cells by western blotting. Results of (B) Cell Counting Kit-8 assay, (C) colony formation assay, (D) Transwell assay and (E) wound healing assay after knockout of METTL5 in SCC15 cells. *P<0.05, **P<0.01; ***P<0.001; ****P<0.0001. METTL5, methyltransferase 5, N6-adenosine; NC, negative control; OSCC, oral squamous cell carcinoma; sg, small guide RNA; NC, negative control; OD, optical density.
    Figure Legend Snippet: Knockout of METTL5 inhibits the progression of OSCC in vitro . (A) Validation of METTL5 stable knockout in SCC15 cells by western blotting. Results of (B) Cell Counting Kit-8 assay, (C) colony formation assay, (D) Transwell assay and (E) wound healing assay after knockout of METTL5 in SCC15 cells. *P<0.05, **P<0.01; ***P<0.001; ****P<0.0001. METTL5, methyltransferase 5, N6-adenosine; NC, negative control; OSCC, oral squamous cell carcinoma; sg, small guide RNA; NC, negative control; OD, optical density.

    Techniques Used: Knock-Out, In Vitro, Biomarker Discovery, Western Blot, Cell Counting, Colony Assay, Transwell Assay, Wound Healing Assay, Negative Control

    Overexpression of METTL5 promotes the progression of OSCC. (A) Validation of METTL5 overexpression in SCC15 cells by western blotting. (B) Results of the Cell Counting Kit-8 assay after METTL5 overexpression in SCC15 cells. (C) Statistical results of the Transwell assay after METTL5 overexpression in SCC15 cells. (D) Results of the colony formation assay after knockout of METTL5 in SCC15 cells. **P<0.01. METTL5, methyltransferase 5, N6-adenosine; OSCC, oral squamous cell carcinoma; oe, overexpression; NC, negative control; OD, optical density.
    Figure Legend Snippet: Overexpression of METTL5 promotes the progression of OSCC. (A) Validation of METTL5 overexpression in SCC15 cells by western blotting. (B) Results of the Cell Counting Kit-8 assay after METTL5 overexpression in SCC15 cells. (C) Statistical results of the Transwell assay after METTL5 overexpression in SCC15 cells. (D) Results of the colony formation assay after knockout of METTL5 in SCC15 cells. **P<0.01. METTL5, methyltransferase 5, N6-adenosine; OSCC, oral squamous cell carcinoma; oe, overexpression; NC, negative control; OD, optical density.

    Techniques Used: Over Expression, Biomarker Discovery, Western Blot, Cell Counting, Transwell Assay, Colony Assay, Knock-Out, Negative Control

    Inhibition of METTL5 suppresses tumor growth in vivo . (A) Representative images of subcutaneous tumors from the SCC15 cell mouse model. (B) Quantification of tumor weight and tumor volume. (C) Tumor volume changes during treatment. (D) Quantitative analysis of IHC scores for METTL5 and Ki-67 expression. (E) Representative images of METTL5 and Ki-67 staining. **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; sg, small guide RNA; NC, negative control; IHC, immunohistochemistry.
    Figure Legend Snippet: Inhibition of METTL5 suppresses tumor growth in vivo . (A) Representative images of subcutaneous tumors from the SCC15 cell mouse model. (B) Quantification of tumor weight and tumor volume. (C) Tumor volume changes during treatment. (D) Quantitative analysis of IHC scores for METTL5 and Ki-67 expression. (E) Representative images of METTL5 and Ki-67 staining. **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; sg, small guide RNA; NC, negative control; IHC, immunohistochemistry.

    Techniques Used: Inhibition, In Vivo, Expressing, Staining, Negative Control, Immunohistochemistry

    Knockout of METTL5 selectively inhibits the translation of oncogenic mRNAs. (A) TE scatter plot of METTL5 knockout and control SCC15 cells. (B) Pathway enrichment of TE-downregulated genes. (C) Western blotting confirmed the decreased protein levels of CCND3 in METTL5 knockout SCC15 cells. METTL5, methyltransferase 5, N6-adenosine; TE, translation efficiency; CCND3, cyclin D3; sg, small guide RNA; NC, negative control.
    Figure Legend Snippet: Knockout of METTL5 selectively inhibits the translation of oncogenic mRNAs. (A) TE scatter plot of METTL5 knockout and control SCC15 cells. (B) Pathway enrichment of TE-downregulated genes. (C) Western blotting confirmed the decreased protein levels of CCND3 in METTL5 knockout SCC15 cells. METTL5, methyltransferase 5, N6-adenosine; TE, translation efficiency; CCND3, cyclin D3; sg, small guide RNA; NC, negative control.

    Techniques Used: Knock-Out, Control, Western Blot, Negative Control



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    TRMT112 was highly expressed in <t>OSCC</t> and associated with poor prognosis. (A) qPCR analysis showed that TRMT1 12 mRNA was significantly increased in OSCC tissues compared to matched adjacent non-tumor tissues. (B) qPCR analysis revealed that TRMT1 12 mRNA was highly expressed in OSCC cell lines when compared to normal oral keratinocyte cell line. (C) TRMT1 12 mRNA was significantly overexpressed in the OSCC-TCGA dataset. (D) TRMT1 12 mRNA was significantly overexpressed in the HNSCC-TCGA dataset. (E, F) Kaplan-Meier and log-rank testing showed the prognosis of the patient cohort (overall and disease-free survival).
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    A A model of oral carcinogenesis was established in mice by 4-NQO drinking water. B Representative images of tongue specimens from mice collected at weeks 16, 26, and 32. C The statistical graph shows the percentage of patients with lymph node metastasis. D HE staining of tumor tissues and normal tissues. E The results of IHC staining show the levels of USP25 in the indicated groups. F The expression of USP25 in normal tissue, dysplasia tissue, and tumor tissue are shown. G Western blot analysis of the <t>SCC15</t> and SCC25 cell lines. H CCK8 assays for the SCC15 and SCC25 cell lines. I Wound-healing assays for HNSCC cells overexpressing USP25. J Transwell assays for HNSCC cells with USP25 overexpression. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.
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    METTL5 is elevated in HNSCC and is associated with poor prognosis of HNSCC. (A) Comparison of mRNA levels of METTL5 in HNSCC with normal tissues in TCGA-HNSCC dataset. (B) Overall survival of patients between METTL5-high (n=259) and METTL5-low (n=259) groups. (C) METTL5 expression level in normal and HNSCC tissues with different stages of lymph node metastasis. (D) METTL5 expression level in normal tissues and different stages of HNSCC tissues. (E) METTL5 expression level in normal HNSCC tissues and different grades of HNSCC tissues. (F) METTL5 protein level in OSCC(HSC3, SCC15) and HOK cell lines. (G) Representative bands of METTL5 protein expression levels in human OSCC and paired normal tissues measured by western blotting. (H) Semi-quantification of METTL5 protein expression levels in human OSCC and paired normal tissues. *P<0.05, **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; HNSCC, head and neck squamous cell carcinoma; TCGA, The Cancer Genome Atlas; OSCC, oral squamous cell carcinoma; HOK, human normal oral epithelial keratinocyte; HR, hazard ratio; TPM, transcripts per million; N, normal; T, tumor.

    Journal: Oncology Letters

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    doi: 10.3892/ol.2026.15490

    Figure Lengend Snippet: METTL5 is elevated in HNSCC and is associated with poor prognosis of HNSCC. (A) Comparison of mRNA levels of METTL5 in HNSCC with normal tissues in TCGA-HNSCC dataset. (B) Overall survival of patients between METTL5-high (n=259) and METTL5-low (n=259) groups. (C) METTL5 expression level in normal and HNSCC tissues with different stages of lymph node metastasis. (D) METTL5 expression level in normal tissues and different stages of HNSCC tissues. (E) METTL5 expression level in normal HNSCC tissues and different grades of HNSCC tissues. (F) METTL5 protein level in OSCC(HSC3, SCC15) and HOK cell lines. (G) Representative bands of METTL5 protein expression levels in human OSCC and paired normal tissues measured by western blotting. (H) Semi-quantification of METTL5 protein expression levels in human OSCC and paired normal tissues. *P<0.05, **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; HNSCC, head and neck squamous cell carcinoma; TCGA, The Cancer Genome Atlas; OSCC, oral squamous cell carcinoma; HOK, human normal oral epithelial keratinocyte; HR, hazard ratio; TPM, transcripts per million; N, normal; T, tumor.

    Article Snippet: SCC15 cells were purchased from the American Type Culture Collection (cat. no. CRL-1623).

    Techniques: Comparison, Expressing, Western Blot

    Knockout of METTL5 inhibits the progression of OSCC in vitro . (A) Validation of METTL5 stable knockout in SCC15 cells by western blotting. Results of (B) Cell Counting Kit-8 assay, (C) colony formation assay, (D) Transwell assay and (E) wound healing assay after knockout of METTL5 in SCC15 cells. *P<0.05, **P<0.01; ***P<0.001; ****P<0.0001. METTL5, methyltransferase 5, N6-adenosine; NC, negative control; OSCC, oral squamous cell carcinoma; sg, small guide RNA; NC, negative control; OD, optical density.

    Journal: Oncology Letters

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    doi: 10.3892/ol.2026.15490

    Figure Lengend Snippet: Knockout of METTL5 inhibits the progression of OSCC in vitro . (A) Validation of METTL5 stable knockout in SCC15 cells by western blotting. Results of (B) Cell Counting Kit-8 assay, (C) colony formation assay, (D) Transwell assay and (E) wound healing assay after knockout of METTL5 in SCC15 cells. *P<0.05, **P<0.01; ***P<0.001; ****P<0.0001. METTL5, methyltransferase 5, N6-adenosine; NC, negative control; OSCC, oral squamous cell carcinoma; sg, small guide RNA; NC, negative control; OD, optical density.

    Article Snippet: SCC15 cells were purchased from the American Type Culture Collection (cat. no. CRL-1623).

    Techniques: Knock-Out, In Vitro, Biomarker Discovery, Western Blot, Cell Counting, Colony Assay, Transwell Assay, Wound Healing Assay, Negative Control

    Overexpression of METTL5 promotes the progression of OSCC. (A) Validation of METTL5 overexpression in SCC15 cells by western blotting. (B) Results of the Cell Counting Kit-8 assay after METTL5 overexpression in SCC15 cells. (C) Statistical results of the Transwell assay after METTL5 overexpression in SCC15 cells. (D) Results of the colony formation assay after knockout of METTL5 in SCC15 cells. **P<0.01. METTL5, methyltransferase 5, N6-adenosine; OSCC, oral squamous cell carcinoma; oe, overexpression; NC, negative control; OD, optical density.

    Journal: Oncology Letters

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    doi: 10.3892/ol.2026.15490

    Figure Lengend Snippet: Overexpression of METTL5 promotes the progression of OSCC. (A) Validation of METTL5 overexpression in SCC15 cells by western blotting. (B) Results of the Cell Counting Kit-8 assay after METTL5 overexpression in SCC15 cells. (C) Statistical results of the Transwell assay after METTL5 overexpression in SCC15 cells. (D) Results of the colony formation assay after knockout of METTL5 in SCC15 cells. **P<0.01. METTL5, methyltransferase 5, N6-adenosine; OSCC, oral squamous cell carcinoma; oe, overexpression; NC, negative control; OD, optical density.

    Article Snippet: SCC15 cells were purchased from the American Type Culture Collection (cat. no. CRL-1623).

    Techniques: Over Expression, Biomarker Discovery, Western Blot, Cell Counting, Transwell Assay, Colony Assay, Knock-Out, Negative Control

    Inhibition of METTL5 suppresses tumor growth in vivo . (A) Representative images of subcutaneous tumors from the SCC15 cell mouse model. (B) Quantification of tumor weight and tumor volume. (C) Tumor volume changes during treatment. (D) Quantitative analysis of IHC scores for METTL5 and Ki-67 expression. (E) Representative images of METTL5 and Ki-67 staining. **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; sg, small guide RNA; NC, negative control; IHC, immunohistochemistry.

    Journal: Oncology Letters

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    doi: 10.3892/ol.2026.15490

    Figure Lengend Snippet: Inhibition of METTL5 suppresses tumor growth in vivo . (A) Representative images of subcutaneous tumors from the SCC15 cell mouse model. (B) Quantification of tumor weight and tumor volume. (C) Tumor volume changes during treatment. (D) Quantitative analysis of IHC scores for METTL5 and Ki-67 expression. (E) Representative images of METTL5 and Ki-67 staining. **P<0.01; ***P<0.001. METTL5, methyltransferase 5, N6-adenosine; sg, small guide RNA; NC, negative control; IHC, immunohistochemistry.

    Article Snippet: SCC15 cells were purchased from the American Type Culture Collection (cat. no. CRL-1623).

    Techniques: Inhibition, In Vivo, Expressing, Staining, Negative Control, Immunohistochemistry

    Knockout of METTL5 selectively inhibits the translation of oncogenic mRNAs. (A) TE scatter plot of METTL5 knockout and control SCC15 cells. (B) Pathway enrichment of TE-downregulated genes. (C) Western blotting confirmed the decreased protein levels of CCND3 in METTL5 knockout SCC15 cells. METTL5, methyltransferase 5, N6-adenosine; TE, translation efficiency; CCND3, cyclin D3; sg, small guide RNA; NC, negative control.

    Journal: Oncology Letters

    Article Title: METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation

    doi: 10.3892/ol.2026.15490

    Figure Lengend Snippet: Knockout of METTL5 selectively inhibits the translation of oncogenic mRNAs. (A) TE scatter plot of METTL5 knockout and control SCC15 cells. (B) Pathway enrichment of TE-downregulated genes. (C) Western blotting confirmed the decreased protein levels of CCND3 in METTL5 knockout SCC15 cells. METTL5, methyltransferase 5, N6-adenosine; TE, translation efficiency; CCND3, cyclin D3; sg, small guide RNA; NC, negative control.

    Article Snippet: SCC15 cells were purchased from the American Type Culture Collection (cat. no. CRL-1623).

    Techniques: Knock-Out, Control, Western Blot, Negative Control

    TRMT112 was highly expressed in OSCC and associated with poor prognosis. (A) qPCR analysis showed that TRMT1 12 mRNA was significantly increased in OSCC tissues compared to matched adjacent non-tumor tissues. (B) qPCR analysis revealed that TRMT1 12 mRNA was highly expressed in OSCC cell lines when compared to normal oral keratinocyte cell line. (C) TRMT1 12 mRNA was significantly overexpressed in the OSCC-TCGA dataset. (D) TRMT1 12 mRNA was significantly overexpressed in the HNSCC-TCGA dataset. (E, F) Kaplan-Meier and log-rank testing showed the prognosis of the patient cohort (overall and disease-free survival).

    Journal: Journal of Oral Biology and Craniofacial Research

    Article Title: High expression of TRMT112 is associated with the development of oral squamous cell carcinoma

    doi: 10.1016/j.jobcr.2025.12.014

    Figure Lengend Snippet: TRMT112 was highly expressed in OSCC and associated with poor prognosis. (A) qPCR analysis showed that TRMT1 12 mRNA was significantly increased in OSCC tissues compared to matched adjacent non-tumor tissues. (B) qPCR analysis revealed that TRMT1 12 mRNA was highly expressed in OSCC cell lines when compared to normal oral keratinocyte cell line. (C) TRMT1 12 mRNA was significantly overexpressed in the OSCC-TCGA dataset. (D) TRMT1 12 mRNA was significantly overexpressed in the HNSCC-TCGA dataset. (E, F) Kaplan-Meier and log-rank testing showed the prognosis of the patient cohort (overall and disease-free survival).

    Article Snippet: CAL27, SCC25, and SCC15 OSCC cell lines were obtained from the American Type Culture Collection (ATCC, USA) and confirmed to be negative for mycoplasma.

    Techniques:

    Protein expression of TRMT112 in OSCC tissues. (A) Western blot analysis showed that TRMT112 protein expression significantly increased in OSCC compared with adjacent non-tumor tissues. (B) HNSCC-TCGA dataset revealed that the expression of TRMT112 was up-regulated in HNSCC tissues compared to normal tissues. (C) Immunohistochemistry analysis also indicated that TRMT112 was highly expressed in tumor tissues when compared to normal tissues.

    Journal: Journal of Oral Biology and Craniofacial Research

    Article Title: High expression of TRMT112 is associated with the development of oral squamous cell carcinoma

    doi: 10.1016/j.jobcr.2025.12.014

    Figure Lengend Snippet: Protein expression of TRMT112 in OSCC tissues. (A) Western blot analysis showed that TRMT112 protein expression significantly increased in OSCC compared with adjacent non-tumor tissues. (B) HNSCC-TCGA dataset revealed that the expression of TRMT112 was up-regulated in HNSCC tissues compared to normal tissues. (C) Immunohistochemistry analysis also indicated that TRMT112 was highly expressed in tumor tissues when compared to normal tissues.

    Article Snippet: CAL27, SCC25, and SCC15 OSCC cell lines were obtained from the American Type Culture Collection (ATCC, USA) and confirmed to be negative for mycoplasma.

    Techniques: Expressing, Western Blot, Immunohistochemistry

    Networks, pathways, and diseases associated with TRMT112. (A, B) TRMT112 protein network. (C) Functional enrichment analysis of the TRMT112 protein interactions associated with cancer-linked pathways. (D) TRMT112 expression positively correlated with METTL5 expression. (E) High expression of METTL5 in OSCC patients (TCGA-OSCC dataset).

    Journal: Journal of Oral Biology and Craniofacial Research

    Article Title: High expression of TRMT112 is associated with the development of oral squamous cell carcinoma

    doi: 10.1016/j.jobcr.2025.12.014

    Figure Lengend Snippet: Networks, pathways, and diseases associated with TRMT112. (A, B) TRMT112 protein network. (C) Functional enrichment analysis of the TRMT112 protein interactions associated with cancer-linked pathways. (D) TRMT112 expression positively correlated with METTL5 expression. (E) High expression of METTL5 in OSCC patients (TCGA-OSCC dataset).

    Article Snippet: CAL27, SCC25, and SCC15 OSCC cell lines were obtained from the American Type Culture Collection (ATCC, USA) and confirmed to be negative for mycoplasma.

    Techniques: Functional Assay, Expressing

    A A model of oral carcinogenesis was established in mice by 4-NQO drinking water. B Representative images of tongue specimens from mice collected at weeks 16, 26, and 32. C The statistical graph shows the percentage of patients with lymph node metastasis. D HE staining of tumor tissues and normal tissues. E The results of IHC staining show the levels of USP25 in the indicated groups. F The expression of USP25 in normal tissue, dysplasia tissue, and tumor tissue are shown. G Western blot analysis of the SCC15 and SCC25 cell lines. H CCK8 assays for the SCC15 and SCC25 cell lines. I Wound-healing assays for HNSCC cells overexpressing USP25. J Transwell assays for HNSCC cells with USP25 overexpression. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Cell Death Discovery

    Article Title: USP25 attenuates the immunosuppressive tumor microenvironment via the deubiquitination of TAB2 in head and neck squamous cell carcinoma

    doi: 10.1038/s41420-025-02883-1

    Figure Lengend Snippet: A A model of oral carcinogenesis was established in mice by 4-NQO drinking water. B Representative images of tongue specimens from mice collected at weeks 16, 26, and 32. C The statistical graph shows the percentage of patients with lymph node metastasis. D HE staining of tumor tissues and normal tissues. E The results of IHC staining show the levels of USP25 in the indicated groups. F The expression of USP25 in normal tissue, dysplasia tissue, and tumor tissue are shown. G Western blot analysis of the SCC15 and SCC25 cell lines. H CCK8 assays for the SCC15 and SCC25 cell lines. I Wound-healing assays for HNSCC cells overexpressing USP25. J Transwell assays for HNSCC cells with USP25 overexpression. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: HNSCC cell lines SCC15 and SCC25 were obtained from the American Type Culture Collection (ATCC, USA).

    Techniques: Staining, Immunohistochemistry, Expressing, Western Blot, Over Expression

    A Volcano plot of the RNA-seq data (red and blue indicate significantly upregulated and downregulated genes, respectively). B Western blot analysis of IL-6 expression in HNSCC cells with USP25 downregulation or overexpression. C ELISA results showing the changes in IL-6 secretion in cell supernatants. D In vitro chemotaxis assay for MDSCs cocultured with SCC15 and SCC25 cells. Scale bar, 100 μm. E KEGG enrichment analysis revealed that MAPK signaling was significantly enriched. F The abundance of c-Jun, P-p38, p38, P-ERK, and ERK was measured by western blotting. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Cell Death Discovery

    Article Title: USP25 attenuates the immunosuppressive tumor microenvironment via the deubiquitination of TAB2 in head and neck squamous cell carcinoma

    doi: 10.1038/s41420-025-02883-1

    Figure Lengend Snippet: A Volcano plot of the RNA-seq data (red and blue indicate significantly upregulated and downregulated genes, respectively). B Western blot analysis of IL-6 expression in HNSCC cells with USP25 downregulation or overexpression. C ELISA results showing the changes in IL-6 secretion in cell supernatants. D In vitro chemotaxis assay for MDSCs cocultured with SCC15 and SCC25 cells. Scale bar, 100 μm. E KEGG enrichment analysis revealed that MAPK signaling was significantly enriched. F The abundance of c-Jun, P-p38, p38, P-ERK, and ERK was measured by western blotting. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: HNSCC cell lines SCC15 and SCC25 were obtained from the American Type Culture Collection (ATCC, USA).

    Techniques: RNA Sequencing, Western Blot, Expressing, Over Expression, Enzyme-linked Immunosorbent Assay, In Vitro, Chemotaxis Assay

    A Proteins were immunoprecipitated from cell lysates with anti-USP25 antibody or anti-TAB2 antibody ( B ) and then analyzed by immunoblotting. C Immunofluorescence of USP25 (red) and TAB2 (green) in HNSCC cells. Scale bar, 20 µm. D Schematic domain structure of USP25 and different mutants. E IP and immunoblot analysis of HEK293T cells transfected with the indicated plasmids. F HEK293T cells were transfected with the indicated plasmids, and proteins were immunoprecipitated with anti-HIS antibody and analyzed by immunoblotting. G The polyubiquitination level of endogenous TAB2 in SCC15 and SCC25 cells stably expressing USP25, catalytically inactive mutant of USP25 (H608A), was measured by an in vitro deubiquitination assay. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Cell Death Discovery

    Article Title: USP25 attenuates the immunosuppressive tumor microenvironment via the deubiquitination of TAB2 in head and neck squamous cell carcinoma

    doi: 10.1038/s41420-025-02883-1

    Figure Lengend Snippet: A Proteins were immunoprecipitated from cell lysates with anti-USP25 antibody or anti-TAB2 antibody ( B ) and then analyzed by immunoblotting. C Immunofluorescence of USP25 (red) and TAB2 (green) in HNSCC cells. Scale bar, 20 µm. D Schematic domain structure of USP25 and different mutants. E IP and immunoblot analysis of HEK293T cells transfected with the indicated plasmids. F HEK293T cells were transfected with the indicated plasmids, and proteins were immunoprecipitated with anti-HIS antibody and analyzed by immunoblotting. G The polyubiquitination level of endogenous TAB2 in SCC15 and SCC25 cells stably expressing USP25, catalytically inactive mutant of USP25 (H608A), was measured by an in vitro deubiquitination assay. Data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: HNSCC cell lines SCC15 and SCC25 were obtained from the American Type Culture Collection (ATCC, USA).

    Techniques: Immunoprecipitation, Western Blot, Immunofluorescence, Transfection, Stable Transfection, Expressing, Mutagenesis, In Vitro