title: Apoptotic function of tumor-associated antigen RCAS1 in oral squamous cell carcinoma.
abstract: BACKGROUND
  Receptor-binding cancer antigen expressed on SiSo cell (RCAS1) is derived from uterine adenocarcinoma and can induce apoptosis in lymphocytes, allowing tumor cells to escape from immune surveillance. RCAS1 is reportedly expressed in a membranous pattern on tumor cell or soluble one in serum of patients. The aim of this study was to investigate expression patterns of RCAS1 and the effect on apoptosis in oral squamous cell carcinoma (OSCC) cell lines.
  
  
  METHODS
  In four kinds of OSCC cell lines (HSC-2, HSC-3, SQUU-A, and SQUU-B), RCAS1 mRNAs and proteins were determined by RT-PCR and immunocytochemistry. Membranous RCAS1 was determined by flow cytometry. Culture supernatants were analyzed for detection of soluble RCAS1 by dot blotting and enzyme-linked immunosorbent assay. Apoptotic ability of RCAS1 on the erythroid leukemia cell line K562 with the putative receptor was evaluated by flow cytometry in co-culture with highly metastatic SQUU-B, with knocked-down RCAS1 cells or in a no-cell contact condition.
  
  
  RESULTS
  RCAS1 mRNA and proteins were expressed in all of OSCC cell lines. Membranous pattern were expressed in all cell lines, while soluble pattern was detected in all supernatants. RCAS1 mRNA, membranous and soluble RCAS1 were significantly seen in SQUU-B more than the other 3 cell lines (P < 0.05). K562 apoptosis was induced in co-culture with each of all cell lines, particularly with SQUU-B. Apoptosis was markedly reduced in co-culture with RCAS1 knockdown cells, but was induced in co-culture without cell contract of SQUU-B.
  
  
  CONCLUSIONS
  Our study suggests that RCAS1 has an apoptotic function via membranous/soluble expression pattern in OSCC cells. RCAS1 may thus affect tumor escape from immune surveillance in OSCC by inducing apoptosis.
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tanaka
authors.affiliation: Division of Maxillofacial Diagnostic and Surgical Sciences, Section of Oral and Maxillofacial Oncology, Faculty of Dental Science, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan. takesea@dent.kyushu-u.ac.jp.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Toyoshima
authors.forename: Kenzo
authors.initials: K
authors.lastname: Sonoda
authors.forename: Ryoji
authors.initials: R
authors.lastname: Kitamura
authors.forename: Masaaki
authors.initials: M
authors.lastname: Sasaguri
authors.forename: Shintaro
authors.initials: S
authors.lastname: Kawano
authors.forename: Ryota
authors.initials: R
authors.lastname: Matsubara
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Goto
authors.forename: Seiji
authors.initials: S
authors.lastname: Nakamura
mesh_terms: D000951:Antigens, Neoplasm / Q000235:genetics / Q000276:immunology*; D017209:Apoptosis / Q000276:immunology*; D002294:Carcinoma, Squamous Cell / Q000276:immunology / Q000473:pathology*; D045744:Cell Line, Tumor; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006801:Humans; D009062:Mouth Neoplasms / Q000276:immunology / Q000473:pathology*; D034741:RNA, Small Interfering; D019139:Tumor Escape
chemical_list: D000951:Antigens, Neoplasm; C120762:EBAG9 protein, human; D034741:RNA, Small Interfering