Open AccessUp‐regulation of CD109 expression is associated with carcinogenesis of the squamous epithelium of the oral cavity
Author(s) -
Hagiwara Sumitaka,
Murakumo Yoshiki,
Sato Tomoko,
Shigetomi Toshio,
Mitsudo Kenji,
Tohnai Iwai,
Ueda Minoru,
Takahashi Masahide
Publication year - 2008
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2008.00949.x
Subject(s) - immunohistochemistry , carcinogenesis , malignant transformation , pathology , cancer , epithelium , esophagus , cell , biology , oral cavity , cancer research , medicine , genetics , orthodontics
CD109 is a glycosylphosphatidylinositol (GPI)–anchored glycoprotein whose expression is up‐regulated in squamous cell carcinomas (SCCs) of the lung, esophagus, and uterus. The purpose of this study was to evaluate CD109 expression in oral tumors, including premalignant lesions, and to assess the clinical application of CD109 in oral cancer. CD109 expression in oral normal and tumor tissues from 124 patients was examined by immunohistochemical staining with anti‐CD109 antibody, and significant relations between clinical features and CD109 expression were statistically assessed. We found that high levels of CD109 expression were frequently detected in SCCs and premalignant lesions of the oral cavity, but not in normal squamous epithelia. The CD109 expression level was higher in well‐differentiated SCCs than in poorly differentiated SCCs. Furthermore, premalignant lesions highly expressing CD109 showed higher risk to progress to SCCs. Oral SCC cell lines overexpressing CD109 exhibited accelerated cell growth in vitro compared with control cell lines. In addition, overexpression of CD109 impaired the transforming growth factor (TGF)–β1‐mediated suppression of cell growth. These findings suggest that CD109 plays a role in the development of oral cancers, and is a useful prognostic marker to predict malignant transformation of premalignant lesions. ( Cancer Sci 2008; 99: 1916–1923)