Oral Oncology
Volume 39, Issue 5 , Pages 515-520, July 2003

Establishment of an oral squamous cell carcinoma cell line with high invasive and p27 degradation activities from a lymph node metastasis

  • Yasusei Kudo

      Affiliations

    • Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
  • ,
  • Shojiro Kitajjma

      Affiliations

    • Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
  • ,
  • Sunao Sato

      Affiliations

    • Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
  • ,
  • Mutsumi Miyauchi

      Affiliations

    • Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
  • ,
  • Ikuko Ogawa

      Affiliations

    • Clinical Laboratory, Hiroshima University Dental Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
  • ,
  • Takashi Takata

      Affiliations

    • Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan
    • Corresponding Author InformationCorresponding author. Tel.: +81-82-257-5634; fax: +81-82-257-5619

Received 11 December 2002; accepted 27 January 2003.

Abstract 

The extent of lymph node metastasis is a major determinant in the prognosis of oral squamous cell carcinoma (OSCC). We present here a new OSCC cell line, MSCC-1, established from a lymph node metastasis of a patient with OSCC of gingiva. First, we examined the expression of p27, p53 and Ki-67 in non-neoplastic mucosa, primary and metastatic cancer lesions by immunohistochemistry. Metastatic cancer cells in the lymph node showed the reduced expression of p27 in comparison with cancer cells in the primary lesion. Cancer celLs both in the primary and metastatic lesions showed overexpression of p53 and Ki-67. Overexpression of p53 and reduced expression of p27 in MSCC-1 cells were also determined by western blot analysis. To characterize MSCC-1 cells, furthermore, we examined the invasive activity and cell proliferation of MSCC-1, comparing with those of other OSCC cell lines, HSC-2 and HSC-3 cells. The invasive capacity of MSCC-1 cells was significant higher than HSC-2 and HSC-3 cells, but cell growth of MSCC-1 cells was slower than HSC-2 and HSC-3 cells. Moreover, we examined the p27 degradation activity by in vitro degradation assay. Interestingly, MSCC-1 cells have the strongest p27 degradation activity among the OSCC cell lines examined. In the present study, we newly established MSCC-1 cells with strong invasiveness and p27 degradation activity from a metastatic lesion. These findings suggest that high activity of p27 degradation may concern with invasiveness of OSCC cells and that MSCC-1 cells can be a useful cell model for studying the detailed mechanism of p27 degradation, invasion and metastasis of OSCC.

Keywords:  Oral squamous cell carcinoma, Cell line, Metastasis, Cell cycle, p27, Ubiquitin, p53, Ki-67

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S1368-8375(03)00015-0

doi:10.1016/S1368-8375(03)00015-0

Oral Oncology
Volume 39, Issue 5 , Pages 515-520, July 2003