BACKGROUND: The purpose of this study is to identify the cellular response ofretinoic acid-treated human oral cancer cell lines. METHODS: Seven human oral cancer cell lines KB, SCC4, SCC9, SCC15, SCC25, OEC-M1, OC1 and OC2 were used for cell culture experiments. Direct cell number counting method was utilized to evaluate cellular response of these human oral cancer cells at the presence or absence of all-trans RA at 1 mM. RESULTS: Through 7-day observation, the cell population of SCC9, SCC15 and SCC25 of RA-treated groups decreased when compared with the non RA-treated groups. These three cell lines were further verified using [3H] thymidine incorporation DNA synthesis assay. KB, SCC4, OC1, OC2 and OEC-M1 cell lines did not show growth inhibition at the presence of RA at 1 mM. CONCLUSIONS: The molecular event of how SCC9, SCC15 and SCC25 are inhibited by RA and how KB, OC1, OC2 and OECM1 are resistant to RA can be further explored on the basis of this study.
BACKGROUND: The purpose of this study is to identify the cellular response ofretinoic acid-treated humanoral cancer cell lines. METHODS: Seven humanoral cancer cell lines KB, SCC4, SCC9, SCC15, SCC25, OEC-M1, OC1 and OC2 were used for cell culture experiments. Direct cell number counting method was utilized to evaluate cellular response of these humanoral cancer cells at the presence or absence of all-trans RA at 1 mM. RESULTS: Through 7-day observation, the cell population of SCC9, SCC15 and SCC25 of RA-treated groups decreased when compared with the non RA-treated groups. These three cell lines were further verified using [3H] thymidine incorporation DNA synthesis assay. KB, SCC4, OC1, OC2 and OEC-M1 cell lines did not show growth inhibition at the presence of RA at 1 mM. CONCLUSIONS: The molecular event of how SCC9, SCC15 and SCC25 are inhibited by RA and how KB, OC1, OC2 and OECM1 are resistant to RA can be further explored on the basis of this study.