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Background: Spindle cell squamous carcinoma (SCSC) is a rare and peculiar biphasic malignant neoplasm that occurs mainly in the upper aerodigestive tract. It consists of sarcomatoid proliferation of pleomorphic spindle-shaped cells and squamous cell carcinoma. Methods: Here, we established a SCSC cell line from a tumour arisen in gingiva. We characterized the feature of a SCSC cell line by immunohistochemistry. To know the biological feature, we examined the cell growth, invasiveness and epithelial-mesenchymal transition markers of a SCSC cell line in comparison with oral squamous cell carcinoma (OSCC) cell lines. Results: By immunohistochemical analyses, the primary tumour expressed cytokeratin and vimentin, indicating carcinosarcoma-like characters. This tumour also showed overexpression of p53 protein. Cultured SCSC cells resulted in bypass of crisis and maintenance over passage 100. The established SCSC cell line was spindle-shaped and showed identical immunohistochemical characters to those of primary tumour cells. Similar to the primary tumour, the cell line showed p53 overexpression and had p53 mutation at codon 132: AAG (lys)→AAT (asp). The SCSC cell line grew slower than two other OSCC cell lines (MSCC-1 and HSC-2), whereas SCSC cells had remarkable invasiveness in comparison with these cell lines. Moreover, SCSC cells expressed wnt-5a and vimentin mRNA at high levels, but did not express E-cadherin mRNA. This expression pattern of the markers was similar to that of mesenchymal cells, not of epithelial cells. Conclusion: In the present study, we newly established a SCSC cell line with strong invasiveness. This is the first report on the establishment of SCSC cell line. The SCSC cell line can be a useful cell model for the study to know the cytodifferentiation and nature of SCSC. [ABSTRACT FROM AUTHOR]

Objective: It is well known that reduction of the cyclin-dependent kinase inhibitor p27[sup Kip1] protein correlates with the malignant behavior of various cancers including oral squamous cell carcinoma (OSCC). The loss of p27[sup Kip1] protein is suggested to be due to the enhancement of its posttranslational degradation. In the present study, to evaluate the effects of p27[sup Kip1] transfection on the cell cycle, we transfected OSCC cell lines with a high activity of p27[sup Kip1] degradation with p27[sup Kip1] threonine 187-to-alanine (T187A) mutant gene, which is not influenced by ubiquitin-mediated degradation, as well as with wild type gene. Methods: We transfected p27[sup Kip1] T187A mutant and wild type gene into OSCC cell lines (HSC2 and HSC3) by using an ecdysone-inducible gene expression system. Results: After treatment with ponasterone A, we could find an induction of both p27[sup Kip1] wild type and T187A mutant protein. Both wild type and T187A mutant protein induced by 5 μM ponasterone A inhibited cell growth and increased cell number at the G1 phase. After treatment with 1 μM ponasterone A, ectopic p27[sup Kip1] protein was degraded in wild type clones, but not in T187A mutant clones. Moreover, transfection of the T187A mutant gene was more effective in inhibiting cell growth even by induction of a small amount of protein. Conclusion: We suggest that the transfection of the p27[sup Kip1] T187A mutant gene can be a modality of cancer gene therapy for OSCC.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]