Browsing by Subject "HNSCC"

Now showing 1 - 3 of 3
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    Cytoplasmic expression of p33ING1b is correlated with tumorigenesis and progression of head and neck squamous cell carcinoma
    (Murcia: F. Hernández, 2011) Li, Xiao-Han; Noguchi, Akira; Nishida, Takeshi; Takahashi, Hiroyuki; Zheng, Yang; Yang, Xiang-Hong; Masuda, Shinji; Kikuchi, Keiji; Takano, Yasuo
    Summary. To clarify the role of p33ING1b in tumorigenesis and progression of head and neck squamous cell carcinoma (HNSCC), we examined the expression and subcellular localization of p33ING1b in 214 HNSCC cases in parallel with 60 dysplasia samples and 48 normal epithelium samples by immunohistochemistry, and analyzed correlations of expression of p33ING1b in HNSCC cases with clinicopathological variables, apototic index and expression of 14-3-3η, p300, p21 and PCNA. Although 12% of HNSCC cases lost expression of p33ING1b, most cases of HNSCC retained expression of p33ING1b with levels similar to those in non-cancerous epithelia. Nuclear expression of p33ING1b was significantly decreased in HNSCC compared to normal epithelia. In contrast, cytoplasmic expression of p33ING1b was found to be significantly higher in HNSCC. An abundance of p33ING1b in cytoplasm positively correlated with poor differentiation and tumor progression. Corresponding to those clinicopathogical features, high expression of p33ING1b in the cytoplasm correlated with PCNA labelling index but in contrast, that in the nuclei correlated with apoptosis. In nuclei, p33ING1b is coexpressed with p300 and p21, implying its roles in tumor suppression. Elevated expression of 14-3-3η was associated with cytoplasmic expression of p33ING1b and immunofluorescence study suggested association of p33ING1b and 14-3-3η. Among three cell lines derived from oral SCC, poorly-differentiated SAS cells showed a relatively high expression of p33ING1b in cytoplasm with
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    Downregulation of nuclear ING3 expression and translocalization to cytoplasm promotes tumorigenesis and progression in head and neck squamous cell carcinoma (HNSCC)
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Li, Xiaohan; Zhang, Qun; Zhang, Mingming; Luo, Yusong
    ING3 (inhibitor of growth gene 3) is a member of the ING gene family, and is considered as a candidate tumor suppressor gene. In order to explore the roles of ING3 in tumorigenesis and cancer progression of head and neck squamous cell carcinoma (HNSCC), ING3 expression was assessed in 173 cases of HNSCC by immunohistochemistry. The expression of ING3 was also compared to clinicopathological variables, and the expression of several tumorigenic markers. Nuclear expression of ING3 in HNSCC was significantly lower than that in dysplasia and normal epithelium, and was negatively correlated with a poor-differentiated status, T staging and TNM staging. In contrast, cytoplasmic expression of ING3 was significantly increased in HNSCC, and was statistically associated with lymph node metastasis and 14-3-3η expression. In addition, nuclear expression of ING3 was positively correlated with the expression of p300, p21 and acetylated p53. In conclusion, decreases in nuclear ING3 may play important roles in tumorigenesis, progression and tumor differentiation in HNSCC. Increases in cytoplasmic ING3 may be due to 14-3-3η binding and may also be involved in malignant progression. Nuclear ING3 may modulate the transactivation of target genes, promoting apoptosis through interactions with p300 and p21. Moreover, ING3 may interact with p300 to upregulate the level of acetylation of p53, and promote p53- mediated cell cycle arrest, senescence and/or apoptosis. Therefore, ING3 may be a potential tumor suppressor and a possible therapeutic target in HNSCC
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    INF-γ sensitizes head and neck squamous cell carcinoma cells to chemotherapy-induced apoptosis and necroptosis through up-regulation of Egr-1
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Xu, Bei; Shu, Yongqian; Liu, Peng
    Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Acquired resistance to standard chemotherapy accounts for most of treatment failure. Here we demonstrate that Interferon-γ (INF-γ) may up-regulate Egr-1 gene expression in HNSCC cell line SCC-25. Forced expression of Egr-1 sensitizes SCC-25 cells to chemotherapy-induced apoptosis and necroptosis, a novel form of programmed cell death. Egr-1 upregulation also significantly increases the production of Thrombospondin-1 (TSP-1), a matricellular glycoprotein which has been described to induce cell death in HNSCC. Moreover, INF-γ-induced sensitization of cells to chemotherapy-mediated cell death and TSP-1 production could be markedly abolished by Egr-1 silencing. The present investigation provides the first evidence that INF-γ may sensitize HNSCC cells to chemotherapy-induced apoptosis and necroptosis through up-regulation of Egr-1. These data support the combination use of INF-γ and cytotoxic drugs for HNSCC Therapy.