S100a7 Regulates Dna Damage-Induced Immunogenicity In Oral Cancer Immunoradiotherapy

Oral cancer incidence continues to increase, but the survival rate and prognosis of patients are improving slowly. Some patients show resistance to traditional chemoradiotherapy and insensitivity to current immunotherapy. Therefore, there is an urgent need for biomarkers to indicate effective treatments for oral cancer patients. Here, we aim to investigate S100A7 as a biomarker in modulating the effect of immunoradiotherapy in oral cancer. The TCGA database was used to analyze the correlation of related genes with survival of oral cancer patients. Tumor tissue micro-array with 119 tumors and 61 normal tissue was used to evaluate S100A7 protein levels and tumor infiltrating immune cells. Oral cancer cell lines were used to investigate the effect of S100A7 in regulating cell response to irradiation. S100A7 mRNA and protein was highly expressed in oral cancer patients. For patients with classical chemoradiotherapy, the high expression of S100A7 gene indicated better prognoses with a higher survival trend. ICH staining of S100A7 protein in tumor tissue array revealed positive correlations of S100A7 with immunosuppressive cells (PD-L1+ cells and Foxp3+ cells, n=119, P=0.0126 and P=0.0073, respectively). The expression level of S100A7 was increased after irradiation in oral cancer cells, and accompanied with an increased immunogenic cytosolic DNA. In this study, we found S100A7 was highly expressed in oral cancer, and positive correlated with tumor infiltrating immunosuppressive cells. Radiation increased S100A7 in oral cancer cells with cytosolic DNA, indicated S100A7 played roles in regulating DNA damage-induced immunogenicity in oral cancer immunoradiotherapy.

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Publication Details

Journal
International Dental Journal
Published
2025-10-01
DOI
https://doi.org/10.1016/j.identj.2025.105901
Primary Topic
S100 Proteins and Annexins
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article
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article

S100a7 Regulates Dna Damage-Induced Immunogenicity In Oral Cancer Immunoradiotherapy

Yongqiang Deng, Weitao Hu, Lin Ma, Xinghan Li
International Dental Journal
S100 Proteins and Annexins
article

S100a7 Regulates Dna Damage-Induced Immunogenicity In Oral Cancer Immunoradiotherapy

Yongqiang Deng, Weitao Hu, Lin Ma, Xinghan Li
article en

Abstract

Oral cancer incidence continues to increase, but the survival rate and prognosis of patients are improving slowly. Some patients show resistance to traditional chemoradiotherapy and insensitivity to current immunotherapy. Therefore, there is an urgent need for biomarkers to indicate effective treatments for oral cancer patients. Here, we aim to investigate S100A7 as a biomarker in modulating the effect of immunoradiotherapy in oral cancer. The TCGA database was used to analyze the correlation of related genes with survival of oral cancer patients. Tumor tissue micro-array with 119 tumors and 61 normal tissue was used to evaluate S100A7 protein levels and tumor infiltrating immune cells. Oral cancer cell lines were used to investigate the effect of S100A7 in regulating cell response to irradiation. S100A7 mRNA and protein was highly expressed in oral cancer patients. For patients with classical chemoradiotherapy, the high expression of S100A7 gene indicated better prognoses with a higher survival trend. ICH staining of S100A7 protein in tumor tissue array revealed positive correlations of S100A7 with immunosuppressive cells (PD-L1+ cells and Foxp3+ cells, n=119, P=0.0126 and P=0.0073, respectively). The expression level of S100A7 was increased after irradiation in oral cancer cells, and accompanied with an increased immunogenic cytosolic DNA. In this study, we found S100A7 was highly expressed in oral cancer, and positive correlated with tumor infiltrating immunosuppressive cells. Radiation increased S100A7 in oral cancer cells with cytosolic DNA, indicated S100A7 played roles in regulating DNA damage-induced immunogenicity in oral cancer immunoradiotherapy.

International Dental JournalVol. 75
Shenzhen University (CN)
Openalex Percentile: Top 71%
S100 Proteins and Annexins
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