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Transforming growth factor β1 dysregulation in a human oral carcinoma tumour progression model
Author(s) -
Hsu S.,
Borke J. L.,
Lewis J. B.,
Singh B.,
Aiken A. C.,
Huynh C. T.,
Schuster G. S.,
Caughman G. B.,
Dickinson D. P.,
Smith A. K.,
Osaki T.,
Wang X. F.
Publication year - 2002
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1046/j.1365-2184.2002.00237.x
Subject(s) - transforming growth factor , cancer research , growth factor , cell growth , biology , phenotype , cell , cell culture , microbiology and biotechnology , receptor , genetics , gene
. A human oral tumour progression model was established that consists of normal epithelial cells and three cell lines representing stages from dysplastic to metastatic cells. To investigate the impact of exogenous transforming growth factor‐β1 on this model system, we analysed the responsiveness of those cells to transforming growth factor‐β1 and explored the potential mechanism underlying the transforming growth factor‐β1 activity. We found that the growth of all cell types, regardless of their stage of tumour progression, is inhibited by transforming growth factor‐β1, although to different degrees. Transforming growth factor‐β1 induced the expression of cyclin‐dependent kinase inhibitors p15 INK4B , p21WAF1/ CIP1 and p27 KIP1 . In contrast, transforming growth factor‐β1 was found to stimulate the invasive potential of one cell type that represents the most advanced stage of tumour phenotype, suggesting that the impact of transforming growth factor‐β1 on functional features of tumour cells other than cellular proliferation may play a significant role in the process of oral tumour progression.

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