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human hnscc cell lines scc15 (ATCC)

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ATCC human hnscc cell lines scc15
Human Hnscc Cell Lines Scc15, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 635 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/scc+15/pm41976369-72-4-15?v=ATCC
Average 96 stars, based on 635 article reviews

human hnscc cell lines scc15 - by Bioz Stars, 2026-07

96/100 stars

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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

Chemotherapy agents upregulate SIA-cIgG expression, and SIA-cIgG inhibition enhances drug efficacy. (A) SIA-cIgG protein expression of PDO 1 after different drug treatments for 6 d (medium and drugs renewed in day 4) by Western blot assay. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L. (B) Fold change of SIA-cIgG protein expression after different drug treatments for 6 days in PDOs, n = 3 (respectively). (C) Representative SIA-cIgG fluorescence microphotographs of HNSCC PDOs after different drug treatments for 6 days (medium and drugs renewed in day 4). CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L; RP215: 20 μg/mL. Scale bar, 50 μm. (D) Representative microphotographs of SIA-cIgG IHC staining in HNSCC tumor tissue, pre- (above) and post- (below) TPF (CDDP, 5-FU and DTX) chemotherapy. Scale bars, 100 μm. (E) Relative cell viability (% of control) of WSU-HN6 and SCC-15 after different drug combination treatments with/without 20 μg/mL RP215 for 48 h, n = 3 (respectively). 20 μg/mL mIgG was used as negative control to RP215. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 nmol/L; PTX: 5 nmol/L. (F) Flow cytometry analysis of AnnexinV/PI staining for indicating cell apoptosis after different drug combinations treatment for 48 h in WSU-HN6 and SCC-15, n = 3 (respectively). (G) Fold change of IGHGc mRNA expression after different drug treatments for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (H) SIA-cIgG, p-SRC Y419, SRC, p-AKT T308, p-AKT S473, and AKT protein expression after different combination treatments for 36 h in WSU-HN6 and SCC-15, n = 3 (respectively). Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Journal: Journal of Translational Internal Medicine

Article Title: Anti-SIA-cIgG enhances chemotherapy effectiveness through PTPN13-regulated tumor stemness in head and neck squamous cell carcinoma

doi: 10.1515/jtim-2026-0040

Figure Lengend Snippet: Chemotherapy agents upregulate SIA-cIgG expression, and SIA-cIgG inhibition enhances drug efficacy. (A) SIA-cIgG protein expression of PDO 1 after different drug treatments for 6 d (medium and drugs renewed in day 4) by Western blot assay. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L. (B) Fold change of SIA-cIgG protein expression after different drug treatments for 6 days in PDOs, n = 3 (respectively). (C) Representative SIA-cIgG fluorescence microphotographs of HNSCC PDOs after different drug treatments for 6 days (medium and drugs renewed in day 4). CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L; RP215: 20 μg/mL. Scale bar, 50 μm. (D) Representative microphotographs of SIA-cIgG IHC staining in HNSCC tumor tissue, pre- (above) and post- (below) TPF (CDDP, 5-FU and DTX) chemotherapy. Scale bars, 100 μm. (E) Relative cell viability (% of control) of WSU-HN6 and SCC-15 after different drug combination treatments with/without 20 μg/mL RP215 for 48 h, n = 3 (respectively). 20 μg/mL mIgG was used as negative control to RP215. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 nmol/L; PTX: 5 nmol/L. (F) Flow cytometry analysis of AnnexinV/PI staining for indicating cell apoptosis after different drug combinations treatment for 48 h in WSU-HN6 and SCC-15, n = 3 (respectively). (G) Fold change of IGHGc mRNA expression after different drug treatments for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (H) SIA-cIgG, p-SRC Y419, SRC, p-AKT T308, p-AKT S473, and AKT protein expression after different combination treatments for 36 h in WSU-HN6 and SCC-15, n = 3 (respectively). Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Article Snippet: HNSCC cell line SCC-15 (RRID: CVCL_1681) was purchased from the American Type Culture Collection (ATCC) in July 2024.

Techniques: Expressing, Inhibition, Western Blot, Fluorescence, Immunohistochemistry, Control, Negative Control, Flow Cytometry, Staining

Anti-SIA-cIgG inhibits HNSCC cell stemness and malignant biological behaviors. (A) Representative fluorescence microphotographs of SIA-cIgG/CD44 staining in HNSCC tumor tissue. Scale bar, 100 μm. (B) Representative fluorescence microphotographs of SIA-cIgG/CD44 staining in HNSCC PDOs. Scale bar, 50 μm. (C) SIA-cIgG and CD44 protein expression of HNSCC tumor tissue by Western blot assay, n = 49. Sample 01 was used as control. (D) Simple linear regression of SIA-cIgG and CD44 protein expression, n = 49. (E) In vitro Extreme Limiting Dilution Analysis (ELDA) of 20 μg/mL mIgG or RP215-treated HNSCC PDOs. (F-I) CD44 (F), OCT4 (G), SOX2 (H) and VIMENTIN (I) mRNA expression after 20 μg/mL or 50 μg/mL RP215 treatment for 48 h, n = 3 (respectively). (J) SIA-cIgG, CD44, OCT4, SOX2, and VIMENTIN protein expression after 20 μg/mL or 50 μg/mL RP215 treatment for 48 h. (K) Cell proliferation rates of 20 μg/ mL or 50 μg/mL RP215 treatment in WSU-HN6 and SCC-15. 12 h after cell seeded was set as 0 h, n = 3 (respectively). (L-O) Colony formation assay (L), in vitro tumorsphere formation assay (M), Transwell migration (N) and invasion (O) of 20 μg/mL or 50 μg/mL RP215 treatment in WSU-HN6 and SCC-15, n = 3 (respectively). Scale bars, M: 250 μm; N-O: 200 μm. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, ** P < 0.001, ns, no significant difference.

Journal: Journal of Translational Internal Medicine

Article Title: Anti-SIA-cIgG enhances chemotherapy effectiveness through PTPN13-regulated tumor stemness in head and neck squamous cell carcinoma

doi: 10.1515/jtim-2026-0040

Figure Lengend Snippet: Anti-SIA-cIgG inhibits HNSCC cell stemness and malignant biological behaviors. (A) Representative fluorescence microphotographs of SIA-cIgG/CD44 staining in HNSCC tumor tissue. Scale bar, 100 μm. (B) Representative fluorescence microphotographs of SIA-cIgG/CD44 staining in HNSCC PDOs. Scale bar, 50 μm. (C) SIA-cIgG and CD44 protein expression of HNSCC tumor tissue by Western blot assay, n = 49. Sample 01 was used as control. (D) Simple linear regression of SIA-cIgG and CD44 protein expression, n = 49. (E) In vitro Extreme Limiting Dilution Analysis (ELDA) of 20 μg/mL mIgG or RP215-treated HNSCC PDOs. (F-I) CD44 (F), OCT4 (G), SOX2 (H) and VIMENTIN (I) mRNA expression after 20 μg/mL or 50 μg/mL RP215 treatment for 48 h, n = 3 (respectively). (J) SIA-cIgG, CD44, OCT4, SOX2, and VIMENTIN protein expression after 20 μg/mL or 50 μg/mL RP215 treatment for 48 h. (K) Cell proliferation rates of 20 μg/ mL or 50 μg/mL RP215 treatment in WSU-HN6 and SCC-15. 12 h after cell seeded was set as 0 h, n = 3 (respectively). (L-O) Colony formation assay (L), in vitro tumorsphere formation assay (M), Transwell migration (N) and invasion (O) of 20 μg/mL or 50 μg/mL RP215 treatment in WSU-HN6 and SCC-15, n = 3 (respectively). Scale bars, M: 250 μm; N-O: 200 μm. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, ** P < 0.001, ns, no significant difference.

Article Snippet: HNSCC cell line SCC-15 (RRID: CVCL_1681) was purchased from the American Type Culture Collection (ATCC) in July 2024.

Techniques: Fluorescence, Staining, Expressing, Western Blot, Control, In Vitro, Colony Assay, Tube Formation Assay, Migration

PTPN13 is a key downstream effector of SIA-cIgG in regulating tumor stemness and chemoresistance. (A) Kaplan-Meier survival analysis of HNSCC patients with high and low PTPN13 expression. High (H) = 124, Low (L) = 121. (B) GSEA Hallmark gene set enrichment analysis in PI3K/AKT pathway of TCGA comparing low versus high PTPN13 expression. (C) Representative fluorescence microphotographs of SIA-cIgG/PTPN13 co-localization in HNSCC tumor tissue. Scale bar, 100 μm. (D) Representative fluorescence microphotographs of SIA-cIgG/PTPN13 co-localization in HNSCC PDOs. Scale bar, 50 μm. (E) PTPN13, SIA-cIgG, CD44, OCT4, SOX2, and VIMENTIN protein expression of PTPN13 knockdown with/without 20 μg/mL RP215 treatment for 48 h. (F) Relative cell viability (% of control) of WSU-HN6 and SCC-15 after different drug treatments with/without PTPN13 knockdown as well as 20 μg/mL RP215 treatment for 48 h. SiNC was used as negative control to siPTPN13, 20 μg/mL mIgG was used as negative control to RP215, n = 3 (respectively). (G) Representative microphotographs of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. Scale bar, 250 μm. (H) PDOs proliferation rates of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. * P < 0.05, *** P < 0.001. (I) In vitro Extreme Limiting Dilution Analysis (ELDA) of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. (J) Representative microphotographs of shNC or shPTPN13 HNSCC PDOs after different drug treatments with/without 20 μg/mL RP215 treatment. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L. Scale bar, 250 μm. (K-N) Drug response curves of CDDP (K), 5-FU (L), DTX (M) and PTX(N) in shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Journal: Journal of Translational Internal Medicine

Article Title: Anti-SIA-cIgG enhances chemotherapy effectiveness through PTPN13-regulated tumor stemness in head and neck squamous cell carcinoma

doi: 10.1515/jtim-2026-0040

Figure Lengend Snippet: PTPN13 is a key downstream effector of SIA-cIgG in regulating tumor stemness and chemoresistance. (A) Kaplan-Meier survival analysis of HNSCC patients with high and low PTPN13 expression. High (H) = 124, Low (L) = 121. (B) GSEA Hallmark gene set enrichment analysis in PI3K/AKT pathway of TCGA comparing low versus high PTPN13 expression. (C) Representative fluorescence microphotographs of SIA-cIgG/PTPN13 co-localization in HNSCC tumor tissue. Scale bar, 100 μm. (D) Representative fluorescence microphotographs of SIA-cIgG/PTPN13 co-localization in HNSCC PDOs. Scale bar, 50 μm. (E) PTPN13, SIA-cIgG, CD44, OCT4, SOX2, and VIMENTIN protein expression of PTPN13 knockdown with/without 20 μg/mL RP215 treatment for 48 h. (F) Relative cell viability (% of control) of WSU-HN6 and SCC-15 after different drug treatments with/without PTPN13 knockdown as well as 20 μg/mL RP215 treatment for 48 h. SiNC was used as negative control to siPTPN13, 20 μg/mL mIgG was used as negative control to RP215, n = 3 (respectively). (G) Representative microphotographs of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. Scale bar, 250 μm. (H) PDOs proliferation rates of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. * P < 0.05, *** P < 0.001. (I) In vitro Extreme Limiting Dilution Analysis (ELDA) of shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. (J) Representative microphotographs of shNC or shPTPN13 HNSCC PDOs after different drug treatments with/without 20 μg/mL RP215 treatment. CDDP: 10 μmol/L; 5-FU: 12 μmol/L; DTX: 5 μmol/L; PTX: 5 μmol/L. Scale bar, 250 μm. (K-N) Drug response curves of CDDP (K), 5-FU (L), DTX (M) and PTX(N) in shNC or shPTPN13 HNSCC PDOs with/without 20 μg/mL RP215 treatment. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Article Snippet: HNSCC cell line SCC-15 (RRID: CVCL_1681) was purchased from the American Type Culture Collection (ATCC) in July 2024.

Techniques: Expressing, Fluorescence, Knockdown, Control, Negative Control, In Vitro

Anti-SIA-cIgG enhances PTPN13 protein stability. (A) Fold change of PTPN13 mRNA expression after 20 μg/mL or 50 μg/mL of RP215 treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (B) PTPN13 protein expression after treatments of different drugs at different concentration for 48 h in WSU-HN6 and SCC-15. (C) Fold change of PTPN13 mRNA expression after different drugs treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (D) PTPN13 protein expression of WSU-HN6 and SCC-15 after different drugs treatment with/without 20 μg/mL RP215 for 48 h. (E) Binding of PTPN13 to SIA-cIgG in WSU-HN6 and SCC-15 determined by IP. (F, G) CHX chase assay for indicating PTPN13 protein half-life time in WSU-HN6 (F) and SCC-15 (G). After different drugs treatment for 24 h, 50 μg/mL CHX was added into WSU-HN6 or SCC-15 cells for 0, 4, 8, 12 h, Western blot assay was performed to observe PTPN13 protein expression. (H) Ubiquitin protein expression of PTPN13 in WSU-HN6 after different drugs treatment with/without 20 μg/mL RP215 for 24 h, followed by MG132 treatment for 6 h. MG132: 10 μmol/L. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Journal: Journal of Translational Internal Medicine

Article Title: Anti-SIA-cIgG enhances chemotherapy effectiveness through PTPN13-regulated tumor stemness in head and neck squamous cell carcinoma

doi: 10.1515/jtim-2026-0040

Figure Lengend Snippet: Anti-SIA-cIgG enhances PTPN13 protein stability. (A) Fold change of PTPN13 mRNA expression after 20 μg/mL or 50 μg/mL of RP215 treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (B) PTPN13 protein expression after treatments of different drugs at different concentration for 48 h in WSU-HN6 and SCC-15. (C) Fold change of PTPN13 mRNA expression after different drugs treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (D) PTPN13 protein expression of WSU-HN6 and SCC-15 after different drugs treatment with/without 20 μg/mL RP215 for 48 h. (E) Binding of PTPN13 to SIA-cIgG in WSU-HN6 and SCC-15 determined by IP. (F, G) CHX chase assay for indicating PTPN13 protein half-life time in WSU-HN6 (F) and SCC-15 (G). After different drugs treatment for 24 h, 50 μg/mL CHX was added into WSU-HN6 or SCC-15 cells for 0, 4, 8, 12 h, Western blot assay was performed to observe PTPN13 protein expression. (H) Ubiquitin protein expression of PTPN13 in WSU-HN6 after different drugs treatment with/without 20 μg/mL RP215 for 24 h, followed by MG132 treatment for 6 h. MG132: 10 μmol/L. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Article Snippet: HNSCC cell line SCC-15 (RRID: CVCL_1681) was purchased from the American Type Culture Collection (ATCC) in July 2024.

Techniques: Expressing, Concentration Assay, Binding Assay, Western Blot, Ubiquitin Proteomics

Anti-SIA-cIgG upregulates SP1 expression to activate PTPN13 promoter activity. (A) Correlation analysis from TCGA-HNSCC database showed the transcriptional relevant of PTPN13 and SP1 (Created with GEPIA: http://gepia.cancer-pku.cn/index.html ). (B) SIA-cIgG, PTPN13 and SP1 protein expression of 8 different PDOs by Western blot assay. (C) Simple linear regression of SIA-cIgG protein expression and PTPN13 protein expression (left), SIA-cIgG protein expression and SP1 protein expression (middle), PTPN13 protein expression and SP1 protein expression (right), n = 8. (D) Fold change of SP1 mRNA expression after 20 μg/mL or 50 μg/mL RP215 treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (E) Fold change of PTPN13 mRNA expression after SP1 knockdown with/without 20 μg/mL RP215 for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (F) PTPN13 and SP1 protein expression after SP1 knockdown with/without 20 μg/mL RP215 for 48 h in WSU-HN6 and SCC-15. (G) Fold change of SP1 mRNA expression after different drug treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (H) SP1 protein expression after treatments of different drugs at different concentration for 48 h in WSU-HN6 and SCC-15. (I) SP1 protein expression of WSU-HN6 and SCC-15 after different drugs treatment with/without 20 μg/mL RP215 for 48 h. (J) Three predicted SP1 binding site on PTPN13 promoter by JASPAR ( jaspar.genereg.net ). (K) Binding efficiency of SP1 to different sites in SCC-15. ChIP-qPCR assay was performed, and data are shown as the ratio of immunoprecipitated DNA to total input DNA (%), n = 3 (respectively). (L) Relative luciferase activity in SCC-15 transfected with pGL3-Enhancer-PTPN13-promoter-WT or pGL3-Enhancer-PTPN13-promoter-Mutant 1 or pGL3-Enhancer-PTPN13-promoter-Mutant 2 or pGL3-Enhancer-PTPN13-promoter-Mutant 3, as well as pRL-TK, n = 3. (M) Relative luciferase activity in SCC-15 transfected with pGL3-Enhancer-PTPN13-promoter-WT, siSP1/siNC, and treated with/without 20 μg/mL mIgG, n = 3. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Journal: Journal of Translational Internal Medicine

Article Title: Anti-SIA-cIgG enhances chemotherapy effectiveness through PTPN13-regulated tumor stemness in head and neck squamous cell carcinoma

doi: 10.1515/jtim-2026-0040

Figure Lengend Snippet: Anti-SIA-cIgG upregulates SP1 expression to activate PTPN13 promoter activity. (A) Correlation analysis from TCGA-HNSCC database showed the transcriptional relevant of PTPN13 and SP1 (Created with GEPIA: http://gepia.cancer-pku.cn/index.html ). (B) SIA-cIgG, PTPN13 and SP1 protein expression of 8 different PDOs by Western blot assay. (C) Simple linear regression of SIA-cIgG protein expression and PTPN13 protein expression (left), SIA-cIgG protein expression and SP1 protein expression (middle), PTPN13 protein expression and SP1 protein expression (right), n = 8. (D) Fold change of SP1 mRNA expression after 20 μg/mL or 50 μg/mL RP215 treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (E) Fold change of PTPN13 mRNA expression after SP1 knockdown with/without 20 μg/mL RP215 for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (F) PTPN13 and SP1 protein expression after SP1 knockdown with/without 20 μg/mL RP215 for 48 h in WSU-HN6 and SCC-15. (G) Fold change of SP1 mRNA expression after different drug treatment for 24 h in WSU-HN6 and SCC-15, n = 3 (respectively). (H) SP1 protein expression after treatments of different drugs at different concentration for 48 h in WSU-HN6 and SCC-15. (I) SP1 protein expression of WSU-HN6 and SCC-15 after different drugs treatment with/without 20 μg/mL RP215 for 48 h. (J) Three predicted SP1 binding site on PTPN13 promoter by JASPAR ( jaspar.genereg.net ). (K) Binding efficiency of SP1 to different sites in SCC-15. ChIP-qPCR assay was performed, and data are shown as the ratio of immunoprecipitated DNA to total input DNA (%), n = 3 (respectively). (L) Relative luciferase activity in SCC-15 transfected with pGL3-Enhancer-PTPN13-promoter-WT or pGL3-Enhancer-PTPN13-promoter-Mutant 1 or pGL3-Enhancer-PTPN13-promoter-Mutant 2 or pGL3-Enhancer-PTPN13-promoter-Mutant 3, as well as pRL-TK, n = 3. (M) Relative luciferase activity in SCC-15 transfected with pGL3-Enhancer-PTPN13-promoter-WT, siSP1/siNC, and treated with/without 20 μg/mL mIgG, n = 3. Data are represented as the mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, no significant difference.

Article Snippet: HNSCC cell line SCC-15 (RRID: CVCL_1681) was purchased from the American Type Culture Collection (ATCC) in July 2024.

Techniques: Expressing, Activity Assay, Western Blot, Knockdown, Concentration Assay, Binding Assay, ChIP-qPCR, Immunoprecipitation, Luciferase, Transfection, Mutagenesis

Quetiapine could regulate NAT10-mediated ac4C modification in HNSCC. (A) The mainly potential drugs identified by L1000FWD database. (B) The chemical structure of quetiapine. (C) Molecular docking of NAT10 and quetiapine. (D) The binding sensorgram of the interactions between NAT10 and quetiapine. (E) The protein expression of NAT10 was detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.001, <0.001, and 0.002, respectively. (F) The mRNA expression of NAT10 in HNSCC cells; n=3. From left to right, P=0.03, 0.002, and 0.08, respectively. (G) The protein expression of NAT10 after SCC-15 cells were treated with quetiapine was detected through western blotting (left) and quantitatively analyzed (right); n=3. P<0.001. (H) The mRNA expression of NAT10 after SCC-15 cells were treated with quetiapine; n=3. P<0.001. (I) Dot blot assay was conducted to assess the ac4C level. P<0.001. Data are presented as mean ± SD. ns, no significance; *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. EGFR, epidermal growth factor receptor; HDAC, histone deacetylase; HNSCC, head and neck squamous cell carcinoma; MEK, methyl ethyl ketone; MOA, mechanism of action; mRNA, messenger RNA; NF-κB, nuclear factor kappa-B; PARP, poly ADP-ribose polymerase; PLK, polo-like kinase; RAF, Raf kinase; RU, response unit; SD, standard deviation.

Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine could regulate NAT10-mediated ac4C modification in HNSCC. (A) The mainly potential drugs identified by L1000FWD database. (B) The chemical structure of quetiapine. (C) Molecular docking of NAT10 and quetiapine. (D) The binding sensorgram of the interactions between NAT10 and quetiapine. (E) The protein expression of NAT10 was detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.001, <0.001, and 0.002, respectively. (F) The mRNA expression of NAT10 in HNSCC cells; n=3. From left to right, P=0.03, 0.002, and 0.08, respectively. (G) The protein expression of NAT10 after SCC-15 cells were treated with quetiapine was detected through western blotting (left) and quantitatively analyzed (right); n=3. P<0.001. (H) The mRNA expression of NAT10 after SCC-15 cells were treated with quetiapine; n=3. P<0.001. (I) Dot blot assay was conducted to assess the ac4C level. P<0.001. Data are presented as mean ± SD. ns, no significance; *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. EGFR, epidermal growth factor receptor; HDAC, histone deacetylase; HNSCC, head and neck squamous cell carcinoma; MEK, methyl ethyl ketone; MOA, mechanism of action; mRNA, messenger RNA; NF-κB, nuclear factor kappa-B; PARP, poly ADP-ribose polymerase; PLK, polo-like kinase; RAF, Raf kinase; RU, response unit; SD, standard deviation.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: Modification, Binding Assay, Expressing, Western Blot, Dot Blot, Histone Deacetylase Assay, Standard Deviation

Quetiapine treatment inhibited HNSCC malignant phenotypes in vitro . (A) CCK-8 assay showed that quetiapine treatment inhibited the proliferation of SCC-15 cells; n=5. P<0.001. (B) Representative images of SCC-15 clones treated with quetiapine using crystal violet solution staining. (C) The quantitation of colony number for SCC-15 cells treated with quetiapine; n=3. P=0.001. (D,E) Apoptosis assay results of SCC-15 cells treated with quetiapine; n=3. P=0.02. (F) Representative imaged of SCC-15 transwell migration treated with quetiapine using crystal violet solution staining. (G) Quantified of transwell migration in SCC-15 cells treated with quetiapine; n=3. P=0.003. (H,I) Wound healing assays showed the treatment of quetiapine inhibited migration of SCC-15 cells. The migration distance was quantified at 24 hours after scratching; n=3. P<0.001. *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. CCK-8, Cell Counting Kit-8; FITC, fluorescein isothiocyanate; HNSCC, head and neck squamous cell carcinoma; PI, propidium iodide.

Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine treatment inhibited HNSCC malignant phenotypes in vitro . (A) CCK-8 assay showed that quetiapine treatment inhibited the proliferation of SCC-15 cells; n=5. P<0.001. (B) Representative images of SCC-15 clones treated with quetiapine using crystal violet solution staining. (C) The quantitation of colony number for SCC-15 cells treated with quetiapine; n=3. P=0.001. (D,E) Apoptosis assay results of SCC-15 cells treated with quetiapine; n=3. P=0.02. (F) Representative imaged of SCC-15 transwell migration treated with quetiapine using crystal violet solution staining. (G) Quantified of transwell migration in SCC-15 cells treated with quetiapine; n=3. P=0.003. (H,I) Wound healing assays showed the treatment of quetiapine inhibited migration of SCC-15 cells. The migration distance was quantified at 24 hours after scratching; n=3. P<0.001. *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. CCK-8, Cell Counting Kit-8; FITC, fluorescein isothiocyanate; HNSCC, head and neck squamous cell carcinoma; PI, propidium iodide.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: In Vitro, CCK-8 Assay, Clone Assay, Staining, Quantitation Assay, Apoptosis Assay, Migration, Cell Counting

Quetiapine treatment inhibited the process of OXPHOS. (A) The mRNA expression of OXPHOS related genes after SCC-15 cells were treated with quetiapine; n=3. From left to right, P values <0.001, <0.001, <0.001, 0.02, <0.001, 0.003, 0.004, <0.001, and <0.001, respectively. (B) The protein expression of OXPHOS related proteins after SCC-15 cells were treated with quetiapine were detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.002, <0.001, <0.001, 0.01, and 0.003, respectively. (C) OCR, which reflects mitochondrial respiration, was decreased in quetiapine treated SCC-15 cells. (D) Statistical chart of OCR various parameters about SCC-15 cells after treated with quetiapine; n=3. From left to right, P values <0.001, 0.002, 0.64, <0.001, and 0.07, respectively. ns, no significance; *, P<0.05, **, P<0.01; ***, P<0.005 by unpaired t -test. mRNA, messenger RNA; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; OCR, oxygen consumption rate; OXPHOS, oxidative phosphorylation.

Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine treatment inhibited the process of OXPHOS. (A) The mRNA expression of OXPHOS related genes after SCC-15 cells were treated with quetiapine; n=3. From left to right, P values <0.001, <0.001, <0.001, 0.02, <0.001, 0.003, 0.004, <0.001, and <0.001, respectively. (B) The protein expression of OXPHOS related proteins after SCC-15 cells were treated with quetiapine were detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.002, <0.001, <0.001, 0.01, and 0.003, respectively. (C) OCR, which reflects mitochondrial respiration, was decreased in quetiapine treated SCC-15 cells. (D) Statistical chart of OCR various parameters about SCC-15 cells after treated with quetiapine; n=3. From left to right, P values <0.001, 0.002, 0.64, <0.001, and 0.07, respectively. ns, no significance; *, P<0.05, **, P<0.01; ***, P<0.005 by unpaired t -test. mRNA, messenger RNA; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; OCR, oxygen consumption rate; OXPHOS, oxidative phosphorylation.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: Expressing, Western Blot, Phospho-proteomics

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