HMGI family expression in human oral squamous carcinoma cell lines and tissues

  • MIYAZAWA Jun
    Department of Oral and Maxillofacial Surgery I, Graduate School of Dentistry, Nippon Dental University at Tokyo
  • SHIRAKAWA Masayori
    Department of Oral and Maxillofacial Surgery I, Graduate School of Dentistry, Nippon Dental University at Tokyo
  • IMAI Kazushi
    Department of Biochemistry, School of Dentistry, Nippon Dental University at Tokyo
  • SANADA Kazuo
    Department of Biochemistry, School of Dentistry, Nippon Dental University at Tokyo

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  • ヒト口腔へん平上皮がん細胞株および組織におけるHMGIファミリーの発現

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Abstract

Expression of mesenchymal marker genes in carcinoma cells contributes to the progression of neoplasms. The HMGI family, consisting of HMGIC, HMGI, and HMGY, binds to transcription factors in enhanceosomes and regulates mesenchymal cell growth. Although aberrant expression of HMGIC initiates mesenchymal tumor formation, the expression of this marker gene in squamous cell carcinomas of the oral cavity has not been investigated previously. The present study was conducted to analyze expression patterns of the HMGI family in oral carcinomas. Elevated expression of HMGIC on conventional reverse transcription polymerase chain reaction (RT-PCR) was observed only in carcinoma cell lines and tissues but not in their normal counterparts. Quantitative analysis of expression levels by real-time RT-PCR demonstrated that HMGIC is up-regulated in E-cadherin-expressing cell lines. Immunohistochemical studies of carcinoma tissue sections found that HMGIC was localized in E-cadherin-positive carcinoma cells, whereas at the invasion front HMGIC was present in PCNA-positive carcinoma cells located at periphery of carcinoma cell nests and in surrounding fibroblast-like cells. The percentage of HMGIC-positive carcinoma cells decreased in poorly differentiated tumor tissue. The percentage of HMGIC-positive cases at the invasive front significantly increased in patients with cervical lymph node metastasis. These results suggest that HMGIC may have a role in the phenotypic alteration of carcinoma cells and the progression of oral carcinomas.

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